How Sugar is Refined - the Basic

Raw sugar is made in tropical countries where sugar cane can be grown profitably. It is then shipped in bulk to a refinery in the country where the sugar is required. It now has to be finally cleaned up, purified and made ready for the consumer.

Sugar Refining Concept

It helps to think of refining as a series of steps from left to right where colour and non-sugars are concentrating to the left and pure sugar is concentrating to the right. However the raw sugar comes into the process to the left of centre, not at one end. In the description that follows the flow of sugar is followed first and then the remainder of the process is reviewed.

The first stage of processing the raw sugar is to soften and then remove the layer of mother liquor surrounding the crystals with a process called “affination”. The raw sugar is mixed with a warm, concentrated syrup of slightly higher purity than the syrup layer so that it will not dissolve the crystals. The resulting magma is centrifuged to separate the crystals from the syrup thus removing the greater part of the impurities from the input sugar and leaving the crystals ready for dissolving before further treatment.The liquor which results from dissolving the washed crystals still contains some colour, fine particles, gums and resins and other non-sugars.

Carbonatation Carbonatation
The first stage of processing the liquor is aimed at removing the solids which make the liquor turbid. Coincidentally some of the colour is removed too. One of the two common processing techniques is known as carbonatation where small clumps of chalk are grown in the juice. The clumps, as they form, collect a lot of the non-sugars so that by filtering out the chalk one also takes out the non-sugars. Once this is done, the sugar liquor is now ready for decolourisation. The other technique, phosphatation, is chemically similar but uses phosphate rather than carbonate formation.

There are also two common methods of colour removal in refineries, both relying on absorption techniques with the liquor being pumped through columns of medium. One option open to the refiner is to use granular activated carbon [GAC] which removes most colour but little else. The carbon is regenerated in a hot kiln where the colour is burnt off from the carbon. The other option is to use an ion exchange resin which removes less colour than GAC but also removes some of the inorganics present. The resin is regenerated chemically which gives rise to large quantities of unpleasant liquid effluents.
The clear, lightly coloured liquor is now ready for crystallisation except that it is a little too dilute for optimum energy consumption in the refinery. It is therefore evaporated prior to going to the crystallisation pan.

Vacuum Pan Boiling
In the pan even more water is boiled off until conditions are right for sugar crystals to grow. You may have done something like this at school but probably not with sugar because it is difficult to get the crystals to grow well. In the factory the workers throw in some sugar dust to initiate crystal formation. Once the crystals have grown the resulting mixture of crystals and mother liquor is spun in centrifuges to separate the two, rather like washing is spin dried. The crystals are then given a final dry with hot air before being packed and/or stored ready for despatch.

The liquor left over from the preparation of white sugar and the washings from the affination stage both contain sugar which it is economic to recover. They are therefore sent to the recovery house which operates rather like a raw sugar factory, aiming to make a sugar with a quality comparable to the washed raws after the affination stage. As with the other sugar processes, one cannot get all of the sugar out of the liquor and therefore there is a sweet by-product made: refiners’ molasses. This is usually turned into a cattle food or is sent to a distillery where alcohol is made.
Source: Illovo
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How Beet Sugar is Made - the Basic 

White beet sugar is made from the beets in a single process, rather than the two steps involved with cane sugar.

The beets are harvested in the autumn and early winter by digging them out of the ground. They are usually transported to the factory by large trucks because the transport distances involved are greater than in the cane industry. This is a direct result of sugar beet being a rotational crop which requires nearly 4 times the land area of the equivalent cane crop which is grown in mono-culture. Because the beets have come from the ground they are much dirtier than sugar cane and have to be thoroughly washed and separated from any remaining beet leaves, stones and other trash material before processing.
Sugar Beet

The processing starts by slicing the beets into thin chips. This process increases the surface area of the beet to make it easier to extract the sugar. The extraction takes place in a diffuser where the beet is kept in contact with hot water for about an hour. Diffusion is the process by which the colour and flavour of tea comes out of the tea leaves in a teapot but a typical diffuser weighs several hundred tons when full of beet and extraction water. The diffuser is a large horizontal or vertical agitated tank in which the beets slices slowly work their way from one end to the other and the water is moved in the opposite direction. This is called counter-current flow and as the water goes it becomes a stronger and stronger sugar solution usually called juice. Of course it also collects a lot of other chemicals from the flesh of the sugar beet.

The exhausted beet slices from the diffuser are still very wet and the water in them still holds some useful sugar. They are therefore pressed in screw presses to squeeze as much juice as possible out of them. This juice is used as part of the water in the diffuser and the pressed beet, by now a pulp, is sent to drying plant where it is turned into pellets which form an important constituent of some animal feeds.

The juice must now be cleaned up before it can be used for sugar production. This is done by a process known as carbonatation where small clumps of chalk are grown in the juice. The clumps, as they form, collect a lot of the non-sugars so that by filtering out the chalk one also takes out the non-sugars. Once this is done the sugar liquor is ready for sugar production except that it is very dilute.The next stage of the process is therefore to evaporate the juice in a multi-stage evaporator. This technique is used because it is an efficient way of using steam and it also creates another, lower grade steam which can be used to drive the crystallisation process.

For this last stage, the syrup is placed into a very large pan, typically holding 60 tons or more of sugar syrup. In the pan even more water is boiled off until conditions are right for sugar crystals to grow. You may have done something like this at school but probably not with sugar because it is difficult to get the crystals to grow well. In the factory the workers usually have to add some sugar dust to initiate crystal formation. Once the crystals have grown the resulting mixture of crystals and mother liquor is spun in centrifuges to separate the two, rather like washing is spin dried. The crystals are then given a final dry with hot air before being packed and/or stored ready for despatch.
Vacuum Pan

The final sugar is white and ready for use, whether in the kitchen or by an industrial user such as a soft drink manufacturer. As for raw sugar production, because one cannot get all the sugar out of the juice, there is a sweet by-product made: beet molasses. This is usually turned into a cattle food or is sent to a fermentation plant such as a distillery where alcohol is made. It does not have the same quality smell and taste as cane molasses so cannot be used for rum production.
Product Sugar

One of the big differences between a beet sugar factory and its cane sugar counterpart is with respect to energy. Both factories need steam and electricity to run and both have co-generation stations where high pressure steam is used to drive turbines which produce the electrical power and create the low pressure steam needed by the process. However the beet factory does not have a suitable by-product to use as fuel for the boilers, it has to burn a fossil fuel such as coal, oil or gas. This is partly because the pulp will not burn properly and partly because the animal feed business has been built from the availability of the pulp.
Power Generation
Source: Illovo
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How Cane Sugar is Made - the 
Basic Story

Cane Field Growing the Cane
Sugar cane is a sub-tropical and tropical crop that prefers lots of sun and lots of water – provided that its roots are not waterlogged. It typically takes about 12 months to reach maturity although the time varies widely around the world from as short as six months in Louisiana to 24 months in some places. Where it differs from many crops is that it re-grows from the roots so the plant lasts many cycles [or ‘ratoons’, a word derived from the Spanish to sprout] before it is worn out.

The More Detail button will take you to the web site of Kew Gardens in a separate window. You should return here when you close that down again.

Bullock Cart Harvesting
Sugar cane is harvested by chopping down the stems but leaving the roots so that it re-grows in time for the next crop. Harvest times tend to be during the dry season and the length of the harvest ranges from as little as 2 ½ months up to 11 months. The cane is taken to the factory: often by truck or rail wagon but sometimes on a cart pulled by a bullock or a donkey!

Mill Roll Extraction
The first stage of processing is the extraction of the cane juice. In many factories the cane is crushed in a series of large roller mills: similar to a mangle [wringer] which was used to squeeze the water out of clean washing a century ago. The sweet juice comes gushing out and the cane fibre is carried away for use in the boilers. In other factories a diffuser is used as is described for beet sugar manufacture. Either way the juice is pretty dirty: the soil from the fields, some small fibres and the green extracts from the plant are all mixed in with the sugar.

Evaporation Evaporation
The factory can clean up the juice quite easily with slaked lime (a relative of chalk) which settles out a lot of the dirt so that it can be sent back to the fields. Once this is done, the juice is thickened up into a syrup by boiling off the water using steam in a process called evaporation. Sometimes the syrup is cleaned up again but more often it just goes on to the crystal-making step without any more cleaning. The evaporation is undertaken in order to improve the energy efficiency of the factory.

Centrifuges Boiling
The syrup is placed into a very large pan for boiling, the last stage. In the pan even more water is boiled off until conditions are right for sugar crystals to grow. You may have done something like this at school but probably not with sugar because it is difficult to get the crystals to grow well. In the factory the workers usually have to throw in some sugar dust to initiate crystal formation. Once the crystals have grown the resulting mixture of crystals and mother liquor is spun in centrifuges to separate the two, rather like washing is spin dried. The crystals are then given a final dry with hot air before being stored ready for despatch.

Raw Sugar Pile Storage
The final raw sugar forms a sticky brown mountain in the store and looks rather like the soft brown sugar found in domestic kitchens. It could be used like that but usually it gets dirty in storage and has a distinctive taste which most people don’t want. That is why it is refined when it gets to the country where it will be used. Additionally, because one cannot get all the sugar out of the juice, there is a sweet by-product made: molasses. This is usually turned into a cattle food or is sent to a distillery where alcohol is made.

Power Generation Power
So what happened to all that fibre from crushing the sugar cane? It is called “bagasse” in the industry. The factory needs electricity and steam to run, both of which are generated using this fibre.The bagasse is burnt in large furnaces where a lot of heat is given out which can be used in turn to boil water and make high pressure steam. The steam is then used to drive a turbine in order to make electricity and create low pressure steam for the sugar making process. This is the same process that makes most of our electricity but there are several important differences

When a large power station produces electricity it burns a fossil fuel [once used, a fuel that cannot be replaced] which contaminates the atmosphere and the station has to dump a lot of low grade heat. All this contributes to global warming. In the cane sugar factory the bagasse fuel is renewable and the gases it produces, essentially CO2, are more than used up by the new cane growing. Add to that the factory use of low grade heat [a system called co-generation] and one can see that a well run cane sugar estate is environmentally friendly.Source: Illovo
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It is thought that cane sugar was first used by man in Polynesia from where it spread to India. In 510 BC the Emperor Darius of what was then Persia invaded India where he found “the reed which gives honey without bees”. The secret of cane sugar, as with many other of man’s discoveries, was kept a closely guarded secret whilst the finished product was exported for a rich profit.

Early Refining in Europe

It was the major expansion of the Arab peoples in the seventh century AD that led to a breaking of the secret. When they invaded Persia in 642 AD they found sugar cane being grown and learnt how sugar was made. As their expansion continued they established sugar production in other lands that they conquered including North Africa and Spain.

Sugar was only discovered by western Europeans as a result of the Crusades in the 11th Century AD. Crusaders returning home talked of this “new spice” and how pleasant it was. The first sugar was recorded in England in 1099. The subsequent centuries saw a major expansion of western European trade with the East, including the importation of sugar. It is recorded, for instance, that sugar was available in London at “two shillings a pound” in 1319 AD. This equates to about US$100 per kilo at today’s prices so it was very much a luxury.

The Caribbean

In the 15th century AD, European sugar was refined in Venice, confirmation that even then when quantities were small, it was difficult to transport sugar as a food grade product. In the same century, Columbus sailed to the Americas, the “New World”. It is recorded that in 1493 he took sugar cane plants to grow in the Caribbean. The climate there was so advantageous for the growth of the cane that an industry was quickly established.

By 1750 there were 120 sugar refineries operating in Britain. Their combined output was only 30,000 tons per annum. At this stage sugar was still a luxury and vast profits were made to the extent that sugar was called “white gold”. Governments recognised the vast profits to be made from sugar and taxed it highly. In Britain for instance, sugar tax in 1781 totalled £326,000, a figure that had grown by 1815 to £3,000,000. This situation was to stay until 1874 when the British government, under Prime Minister Gladstone, abolished the tax and brought sugar prices within the means of the ordinary citizen.

Sugar beet was first identified as a source of sugar in 1747. No doubt the vested interests in the cane sugar plantations made sure that it stayed as no more than a curiosity, a situation that prevailed until the Napoleonic wars at the start of the 19th century when Britain blockaded sugar imports to continental Europe. By 1880 sugar beet had replaced sugar cane as the main source of sugar on continental Europe. Those same vested interests probably delayed the introduction of beet sugar to England until the First World War when Britain’s sugar imports were threatened.

Today’s modern sugar industry is still beset with government interference at many levels and throughout the world. The overall pattern can be seen by investigating the mid 1990s’ position in the interactive map on the , Annual consumption is now running at about 120 million tons and is expanding at a rate of about 2 million tons per annum. The European Union, Brazil and India are the top three producers and together account for some 40% of the annual production. However most sugar is consumed within the country of production and only approximately 25% is traded internationally.

One of the most important examples of governmental actions is within the European Union where sugar prices are so heavily subsidised that over 5 million tons of white beet sugar have to be exported annually and yet a million tons of raw cane sugar are imported from former colonies. This latter activity is a form of overseas aid which is also practised by the USA. The EU’s over-production and subsequent dumping has now been subjected to GATT requirements which should see a substantial cut-back in production over the next few years.

source: Illovo

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Sugar Growing Sugar is made by some plants to store energy that they don’t need straight away, rather like animals make fat. People like sugar for its sweetness and its energy so some of these plants are grown commercially to extract the sugar:

Sugar is produced in 121 Countries and global production now exceeds 120 Million tons a year. Approximately 70% is produced from sugar cane, a very tall grass with big stems which is largely grown in the tropical countries. The remaining 30% is produced from sugar beet, a root crop resembling a large parsnip grown mostly in the temperate zones of the north.

World Map

An interactive World Map of Sugar production. Click on an area to learn more about it!

What we call sugar, the chemist knows as ‘sucrose’, one of the family of sugars otherwise known as saccharides in the grouping called carbohydrates. Carbohydrates, as the name implies, contain carbon and hydrogen plus oxygen in the same ratio as in water. The saccharides is a large family with the general formula CnH2nOn. The simplest of the sugars is glucose, C6H12O6, although its physical chemistry is not that simple because it occurs in two distinct forms which affect some of its properties. Sucrose, C12H22O11, is a disaccharide, a condensation molecule made up of two glucose molecules [less a water molecule to make the chemistry work].

The process whereby plants make sugars is photosynthesis. The plant takes in carbon dioxide from the air though pores in its leaves and absorbs water through its roots. These are combined to make sugar using energy from the sun and with the help of a substance called chlorophyll. Chlorophyll is green which allows it to absorb the sun’s energy more readily and which, of course, gives the plants’ leaves their green colour. The reaction of photosynthesis can be written as the following chemical equation when sucrose is being made:

12 CO2 + 11 H2 O = C12 H22 O11 + 12 O2
carbon dioxide + water = sucrose + oxygen

This shows that oxygen is given off during the process of photosynthesis.

Historically, sugar was only produced from sugar cane and then only in relatively small quantities. This resulted in it being considered a great luxury, particularly in Europe where cane could not be grown. The history of man and sugar is a subject in its own right but suffice to say that, even today, it isn’t easy to ship food quality sugar across the world so a high proportion of cane sugar is made in two stages. Raw sugar is made where the sugar cane grows and white sugar is made from the raw sugar in the country where it is needed. Beet sugar is easier to purify and most is grown where it is needed so white sugar is made in only one stage.

To read more about the history of the industry and see how the various processes work with the final results, the sugar we buy, click on the appropriate. Within each page there are also links to further sites with more detailed information.

Sugar Cane

Sugar Cane
Sugar cane is a genus of tropical grasses which requires strong sunlight and abundant water for satisfactory growth. The Latin names of the species include Saccharum officinarum, S. spontaneum, S. barberi and S. sinense. As with most commercial crops, there are many cultivars available to the cane farmer, usually hybrids of several species. Some varieties grow up to 5 metres tall.

The cane itself looks rather like bamboo cane and it is here that the sucrose is stored. In the right climate the cane will grow in 12 months and, when cut, will re-grow in another 12 months provided the roots are undisturbed.

A typical sugar content for mature cane would be 10% by weight but the figure depends on the variety and varies from season to season and location to location. Equally, the yield of cane from the field varies considerably but a rough and ready overall value to use in estimating sugar production is 100 tons of cane per hectare or 10 tons of sugar per hectare.

Sugar Beet

Sugar Beet
Sugar beet is a temperate climate biennial root crop. It produces sugar during the first year of growth in order to see it over the winter and then flowers and seeds in the second year. It is therefore sown in spring and harvested in the first autumn/early winter. As for sugar cane, there are many cultivars available to the beet farmer. The beet stores the sucrose in the bulbous root which bears a strong resemblance to a fat parsnip.

A typical sugar content for mature beets is 17% by weight but the value depends on the variety and it does vary from year to year and location to location. This is substantially more than the sucrose content of mature cane but the yields of beet per hectare are much lower than for cane so that the expected sugar production is only about 7 tons per hectare.

The World of Sugar Production : Mid 1990’s

AUSTRALIA Australian Flag
Exports: 4.7 million tons
Production: 5.5 million tons
Population: 19 million
Per Capita Consumption: 45 kg

BRAZIL Brazilian Flag
Exports: 6 million tons
Production: 14.5 million tons
Population: 167 million
Per Capita Consumption: 48 kg

E.U. EU Flag
Exports: 5.5 million tons
Production: 18 million tons
Population: 375 million
Per Capita Consumption: 36 kg
India Indian Flag
Exports: 0.5 million tons
Production: 14 million tons
Population: 981 million
Per Capita Consumption: 14 kg

SOUTH AFRICA South African Flag
Exports: 1.1 million tons
Production: 2.5 million tons
Population: 45 million
Per Capita Consumption: 30 kg

Exports: 4 million tons
Production: 6 million tons
Population: 62 million
Per Capita Consumption: 27 kg

USA American Flag
Exports: nil
Production: 6.5 million tons
Population: 269 million
Per Capita Consumption: 30 kg

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Scientifically speaking, sugar is defined as a class of molecules made up of carbon, oxygen, and hydrogen arranged in a ringed structure. It is a part of a grouping called carbohydrates which also include starches, celluloses, and gums produced only by photosynthetic plants. Simple sugar molecules, called saccharides, are the building blocks that form carbohydrates. They are an essential structural component of living cells and the source of energy for all animals, including humans.

Usually when people speak of sugar, they are talking about common table sugar. However, sugar has many names and forms. It is also necessary in the diet. The brain depends on it. So does our level of energy. Unfortunately, mankind is now inundated with the wrong kinds of sugar, as evidenced by skyrocketing heart disease, diabetes, and obesity.

There are dozens of different kinds of sugar under a variety of names:

  • barley malt
  • brown sugar
  • cane sugar
  • corn syrup
  • dextrose
  • fructose
  • fruit sugar
  • glucose
  • high-fructose corn syrup
  • honey
  • icing sugar
  • invert sugar
  • jaggary
  • lactose
  • maltose
  • maple syrup
  • molasses
  • powdered sugar
  • raw sugar
  • rice syrup
  • saccharinose
  • sucrose
  • sugar beets
  • turbinados
  • and more….

There are sugar alcohols as sorbitol, mannitol, and xylitol, to name but three; gum sugars, which are complex polysaccharides found in various vegetables; and sugar substitutes, which are designed for the diabetic and dieter but which can be very harmful to the body. But, we are still not finished.

There are essential sugars, just like there are essential fats. People are consuming too much of the wrong kind of those too. Although vital to health, the types of fats and sugars chosen for us by the food industry are destroying our bodies. It is time to take back the control of our own health and find out just what sugars (and fats) we need to maintain health and which ones we need to avoid.

Using less sugar or using alternatives is not as hard as it sounds. Many resort to commercial sugar substitutes, but these are proving just as harmful as the substance they are trying to eliminate. In fact, in some cases, those substitutes cause more harm than sugar. The following are some healthy alternatives to satisfying that sweet tooth.

  • organic apple or pear sauce as part of the sugar and liquid in a recipe
  • organic apple or plum butter
  • mashed bananas
  • sweet spices, as vanilla, cardamom, ginger, cinnamon, nutmeg, cloves, anise seed
  • organic fruit juices instead of water or milk
  • almond flour instead of a portion of wheat flour
  • reconstituted dried organic fruits
  • sugar pumpkins instead of regular
  • ground nuts instead of wheat in pie crusts
  • frozen grapes, raspberries, blueberries, instead of hard candy snacks

Ann Louise Gittleman, in her book called Get the Sugar Out : 501 Simple Ways to Cut the Sugar Out of Any Diet states,
“Even if you incorporate only one-tenth of the tips in this book, you’re sure to reduce the sugar in your diet and change your life in a positive and noticeable way.”

source: Innvista

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Cellular and Genetic Responses of Plants to Sugar Starvation

Photosynthesis converts solar energy to chemical energy, which then drives the synthesis of sugars from carbon dioxide and water. Sugars play multiple roles in all aspects of plant life. First, they provide the main respiratory substrates for the generation of energy and metabolic intermediates that are then used for the synthesis of macromolecules and other cell constituents. Second, Rib and deoxy-Rib sugars form part of the structure of DNA and RNA. Third, polysaccharides are the major structural elements of plant cell walls. Fourth, linkage to sugar is required for proper functioning of many proteins and lipids. As a consequence, the abundance and depletion of sugars or their derivatives initiate various responses in plants and have profound effects on plant metabolism, growth, and development.

Plants are considered to be carbon autotrophs, but they can be considered as carbon heterotrophs during some part of their life cycle and in some of their non-green organs such roots, stems, and flowers, which are not involved in photosynthesis. Furthermore, carbohydrate depletion can occur and is a fact of life in most plants. For instance, variations in environmental factors such as light, water, or temperature and attacks by pathogens or herbivores may lead to a significant decrease in the efficiency of photosynthesis in source tissues (such as leaves that synthesize and export carbohydrates) and thus reduce the supply of carbohydrates to sink tissues (such as the non-green tissues that import carbohydrates for respiration, growth, and development). Under certain growth conditions, such as during an annual resting season or after leaf shedding, photosynthesis is turned off or operates to a lower degree, and carbohydrate reserves must be utilized and may become limited in nonphotosynthetic tissues. In germinating seeds under unfavorable environmental conditions the mobilization of stores in the cotyledons is delayed, which may result in the depletion of available carbohydrates and a decrease in seedling vigor. Knowledge about the response to sugar starvation and adaptation mechanisms in plants is of both fundamental and agronomic importance.

In nature, the cessation of growth of a heterotrophic living organism is often brought about by a poor nutrient environment, a commonly encountered stress. Environmental changes affect various biochemical reactions, often disturbing the balanced distribution of metabolites within cells. In most instances, living cells show a rapid molecular response to overcome adverse environmental conditions. How a living organism survives during periods of environmental stress is an exciting area of research. The most extensive studies have been done with microorganisms. The ability of microorganisms to sense and respond to unscheduled changes in their environment is crucial to their survival. When cells of microorganisms encounter unfavorable nutrient conditions, they ultimately enter a stationary phase. Cells in the stationary phase are physiologically, biochemically, and morphologically different from cells growing exponentially. Studies using Escherichia coliand yeast (Saccharomyces cerevisiae) have indicated that entry into the stationary phase is a complex, highly regulated process that activates a program for long-term survival. The program includes the lack of a requirement for added nutrients and an absence of cell division. The similarities of eukaryotic and prokaryotic microorganisms in their responses to nutrient limitations suggest that such responses are based on evolutionarily conserved genetic mechanisms.

Similarly, sugar starvation initiates changes in substantial physiological and biochemical processes with the goal of sustaining respiration and other essential metabolic processes in plants. Sugar starvation also initiates changes in cellular processes to recycle cellular constituents and dramatically changes the pattern of gene expression. However, the underlying mechanisms used by plant cells to cope with sugar starvation are largely unknown, and only recently have these questions been addressed experimentally. This lack of knowledge contrasts with the situation in bacteria and yeast, where the molecular biology and physiology of mutants have yielded extensive information about responses to sugar starvation. This review discusses the recent advances made in our understanding of the molecular events that operate in microorganisms upon sugar starvation, as well as the cellular and genetic responses of plants to sugar starvation.


The majority of bacteria spend most of their time in a nutrient-limited starvation phase and as a result have evolved mechanisms that allow them to survive under these conditions and to resume growth once nutrients become available. Some bacteria, e.g.Bacillus spp., undergo major differentiation programs that lead to the formation of highly stress-resistant endospores or cysts. Other bacteria, e.g. E. coli, even without the formation of differentiated cells, enter starvation-induced programs that allow them to survive long periods of non-growth and to restart growth when nutrients become available. These starvation-induced programs often lead to the formation of metabolically less-active cells that are more resistant to a wide range of environmental stresses. This adaptation to starvation conditions is often accompanied by a change in cell size and the induction of genes and stabilization of proteins essential for long-term survival. Evidence suggests that there is a general starvation response among various bacteria species. For example, Glc- or nitrogen-starved cultures of E. coli exhibit resistance to heat or hydrogen peroxide (Jenkins et al., 1988). The nitrogen-fixing bacterium Rhizobium leguminosarum can survive carbon, nitrogen, and phosphorus starvation for at least 2 months with little loss of viability. Upon carbon starvation, R. leguminosarum cells undergo reductive cell division and the levels of protein, DNA, and RNA synthesis decrease to base levels, mRNA stabilizes, and the starved cells are cross-protected against pH, heat, osmotic, and oxidative shock (Thorne and Williams, 1997).

In E. coli, nutrient-starved stationary-phase cells have been used as a model system for studying the molecular mechanism that regulates gene expression under nutrient starvation. Stationary-phase cells have a small spherical shape, are resistant to multiple stresses, synthesize glycogen, and survive long-term starvation. Genes expressed during adaptation to starvation conditions involve several classes of starvation genes that code for special stress-resistant proteins. The two major classes of genes induced upon carbon starvation arecst genes, which require cAMP and enhance the cell’s metabolic potential, and pex genes, which do not require cAMP but play a more direct protective role against stresses (Matin, 1991). A protective role of stress-resistant proteins is proposed due to their ability to rescue misfolded macromolecules (Matin, 1991).

Expression of the stress-resistant proteins depends on an intactrpoS allele (Hengge-Aronis, 1993). However, a common consensus sequence has not been found among various promoters controlled by rpoS, and thus a regulatory cascade that mediates expression of the rpoS-dependent genes has been suggested (Hengge-Aronis, 1993). The protein encoded by rpoSis an alternative ς factor of RNA polymerase and is designated as ςs. Evidence shows that the ςs factors are regulated primarily at the post-transcriptional level by a mechanism that involves a mRNA secondary structure (McCann et al., 1993). In addition, carbon starvation in E. coli might be sensed through the accumulation of homoserine lactone (Huisman and Kolter, 1994).


Stress conditions imposed on yeast can be as diverse as nutrient starvation, suboptimal temperatures or osmolarity, high ethanol concentrations, the presence of heavy metals or oxidation compounds, and desiccation (Ruis and Schüller, 1995). Similarity in response to these stresses has been observed and the previous exposure to one stress generally increases the acquisition of tolerance against challenge by another stress (cross-protection or cross-resistance) (Lewis et al., 1995; Ruis and Schüller, 1995). These observations indicate that cells possess one central molecular mechanism that can be activated by various factors and, upon activation, will protect cells against a number of conditions threatening their survival.

Some carbohydrates or proteins induced by various stresses have been suggested to play a protective role against stresses. For example, a close correlation was observed between the content of trehalose, one of the major reserve carbohydrates in yeast, and the stress resistance of the cells. The levels of trehalose and stress resistance increase rapidly upon exhaustion of Glc in the culture medium (Panek and Panek, 1990). The level of trehalose also increases strongly upon starvation of an essential nutrient such as nitrogen, phosphate, or sulfate in a Glc-containing medium (Attfiel et al., 1992). The same is true during sublethal heat, freeze-thaw, and desiccation treatment (Hottiger et al., 1987; Attfiel et al., 1992). Genes that have been demonstrated to contribute significantly to the ability of yeast cells to survive severe stress include CTT1 (encoding the cytosolic catalase T) and HSP104 and HSP70(encoding heat shock proteins) (Ruis and Schüller, 1995).

How yeast cells respond to a wide range of stresses through a convergent molecular mechanism(s) remains largely unclear. Specific gene control elements and stress-activated transcription factors binding to them are probably shared by the stress-responsive genes. A common feature at the transcriptional level, the stress-response element (STRE), a cis-acting element with the core consensus CCCCT, has been found to be present in the promoters of genes induced by various stresses (Varela et al., 1995). STRE activity correlates well with the potential to establish stress tolerance (Ruis and Schüller, 1995). Msn2p, a transcription factor that activates STRE-regulated genes in response to stress, has been identified. Mutants defective in Msn2p exhibit pleiotrophic hypersensitivity to stress factors (Schmitt and McEntee, 1996). How stress signals are transmitted to STREs is not clear, and this raises the question of whether the various stress factors create a common pathway or multiple pathways that then transmit signals to the stress-specific STREs. STRE activities have been shown to be controlled by the high osmolarity glycerol pathway and the protein kinase A pathway (signaling nutrient stress), suggesting that different signals are transmitted through different pathways (Ruis and Schüller, 1995).

Dramatic morphological changes can be observed in yeast undergoing nutrient starvation. The depletion of nutrients such as carbon, nitrogen, sulfur, or amino acids induces autophagy in yeast (Takeshige et al., 1992). Autophagy is the major route of delivery of cytoplasmic proteins into vacuoles/lysosomes under conditions in which cells require enhanced protein degradation and remodeling of components (Dunn, 1994). A Ser/Thr protein kinase gene, APG1, is essential for both the autophagic process and the maintenance of viability of yeast under starvation conditions (Matsuura et al., 1997). It is therefore hypothesized that autophagy-dependent reconstruction of cellular constituents is required for long-term viability in starvation conditions and that the process involves regulation by protein phosphorylation (Matsuura et al., 1997).


Over the past 20 years, carbohydrate starvation has been studied in a number of plant species. Physiological and cellular changes that occur during a plant’s transition to sugar starvation are most extensively studied in excised maize root tips (Brouquisse et al., 1991; Dieuaide et al., 1992), cultured sycamore cells (Journet et al., 1986; Aubert et al., 1996), and cultured rice suspension cells (Chen et al., 1994). These studies have shown that sugar starvation generally triggers sequential changes in the following cellular events: (a) arrest of cell growth, (b) rapid consumption of cellular carbohydrate content and decrease in respiration rate, (c) degradation of lipids and proteins, (d) increase in accumulation of Pi, phosphorylcholine, and free amino acids, and (e) decline in glycolytic enzymatic activities.

It appears that changes in metabolism are involved in the adaptation response of plant cells to sugar starvation. For example, cells in roots (Brouquisse et al., 1991) and leaves (Peeters and Van Laere, 1992), cultured suspension cells (Journet et al., 1986; Chen et al., 1994), and callus cells (Tassi et al., 1992) modify their metabolism to survive in the absence of sugar. In sugar-starved cultured cells, there is a decrease in enzymatic activities related to sugar metabolism and respiration (Journet et al., 1986; Brouquisse et al., 1991), nitrate reduction and assimilation (Brouquisse et al., 1992), and protein synthesis (Tassi et al., 1992). Decreases in these enzymatic activities presumably protect cells against nutrient stress by switching off biosynthesis (i.e. growth) to conserve energy. At the same time, an increase in enzymatic activities related to catabolism of fatty acids (Dieuaide et al., 1992), amino acids (Brouquisse et al., 1992), and proteins (Tassi et al., 1992) occurs. Such a change can substitute protein and lipid catabolism for sugar catabolism to sustain respiration and metabolic processes (Journet et al., 1986; Brouquisse et al., 1991).

Although these metabolic changes appear to enhance the survival of cultured cells under Glc starvation, they finally result in irreversible damages and cell death (Brouquisse et al., 1991; Chen et al., 1994). Similar metabolic changes occur in plant organs or tissues during senescence or in postharvest situations (Noodén, 1988;King et al., 1990). A common mechanism that regulates metabolic processes during sugar starvation and senescence has been suggested (Noodén, 1988). Sugar starvation has also been described as a component of senescence (Dieuaide et al., 1992).


In Suc-starved sycamore and rice suspension cells, the decline in cellular sugar and starch contents couples with the decline in metabolic activity and the increase in vacuolar autophagic activity (Journet et al., 1986; Chen et al., 1994). Triggering of such autophagic processes presumably involves the regression of cytoplasm, including the organelles, and the recycling of respiratory substrates (Journet et al., 1986; Chen et al., 1994; Aubert et al., 1996). This process is well documented in animal cells (Marzella and Glaumann, 1987) and has been implicated in the nonselective bulk degradation of proteins triggered by nutrient deprivation. Autophagy in plant, animal, and yeast systems is often associated with nutrient starvation. In Suc-provided rice suspension cells, the size of the vacuole is small (Fig. 1a). Vacuolar autophagic activity begins a few hours after Suc starvation, and vacuole size expands either by engulfing neighboring cytoplasm and organelles (except the nucleus) or by vacuoles fusing together (Fig. 1b). After a long period of Suc starvation, the vacuole volume becomes extremely large and the cytoplasm and the leftover organelles (mostly mitochondria) are confined to a narrow area adjacent to cell walls (Fig. 1c). Plant vacuoles are rich in hydrolases, and cytoplasm sequestered by the autophagic vacuoles is eventually degraded by these enzymes. Vacuolar autophagy has also been observed in plants undergoing senescence (Matile and Winkenbach, 1971). Due to the presence of intracellular pools of carbohydrates and the ability to control the autophagic process, plant cells can survive for some time after carbohydrate starvation.

Fig. 1.

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Electron micrographs showing morphological changes of cultured rice suspension cells during Suc starvation. Cells were Suc-starved for 0 d (a), 1 d (b), and 2 d (c), and examined under an electron microscope. AMY, Amyloplast; CW, cell wall; M, mitochondria; N, nucleus; S, starch granule; V, vacuole. Bar = 4 μm.


Sugar plays an important dual role in regulating the expression of various genes in plants. In general, sugar favors the expression of enzymes in connection with biosynthesis, utilization, and storage of reserves (including starch, lipid, and proteins). On the other hand, sugar represses the expression of enzymes involved in photosynthesis and reserve mobilization (Koch, 1996). The events of cellular responses to sugar starvation is shown in Figure 2. Generally, gene expression repressed by sugar is up-regulated by sugar starvation, whereas that enhanced by sugar is down-regulated. The alteration of gene expression by sugar starvation results in the induction of synthesis of preexisting or new proteins and repression of normally expressed proteins.

Fig. 2.

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Events in cellular responses to sugar starvation in plants.

A large and specific set of genes whose expression is induced by sugar starvation has been reported (Koch, 1996). For example, sugar starvation induces the expression of photosynthetic genes in maize mesophyll protoplasts (Sheen, 1990), α-amylase genes in rice suspension cells and germinating embryos (Yu et al., 1991, 1996), Suc synthase (Sh1) gene in maize root tips (Koch et al., 1992), and malate synthase and isocitrate lyse genes in cucumber (Graham et al., 1994). At the beginning of rice seed germination, active metabolism and a rise in the respiration rate cause rapid sugar depletion in the embryo, which then triggers the expression of α-amylase genes and degradation of starch in this tissue (Yu et al., 1996). Sugar depletion is also proposed to be a primary factor in initiating the synthesis of phytohormone GA in the embryo, since sugar reduces the quantity of GA in this tissue (Yu et al., 1996).

Most studies on the mechanisms of sugar repression of gene expression in microorganisms and plants have emphasized regulation at the transcriptional level. In plants, while sugar repression of genes involved in photosynthesis (Sheen, 1990) and the glyoxylate cycle (Graham et al., 1994) operates at the transcriptional level, sugar repression of α-amylase gene expression involves control of transcription and mRNA stability (Sheu et al., 1996; Chan et al., 1994,1998; Lu et al., 1998). Search for cis-regulatory elements in the promoters of sugar-regulated genes is important in understanding the mechanism of sugar regulation of gene expression. Although carbohydrate depletion induces expression of a large set of genes essential for various physiological processes, the cis-acting sugar response elements in the promoters of these genes have not been extensively studied.

A sugar response complex in the promoter region of a Suc-deprivation-induced rice α-amylase gene, αAmy3, has been identified. This complex contains three essential motifs for a high level of sugar-starvation-induced gene expression in rice cells (Lu et al., 1998). One of the motifs, a TATCCA element, along with its variants, are present at a proximity upstream of the transcription start sites of 18 α-amylase genes isolated from various plant species (Yu, 1999) and several other sugar-repressible genes. The TATCCA element is present in tandem repeat between position −116 to −105 of the transcription start site of αAmy3 (Lu et al., 1998). Nuclear proteins from rice suspension cells that bind to the TATCCA element in a sequence-specific and sugar-dependent manner have also been identified (Lu et al., 1998). A 20-bp sequence upstream of the transcription start site of the maize Suc synthase geneShrunken is sufficient to confer sugar inhibition of downstream reporter gene expression (Maas et al., 1990). There is no homology between the sugar response sequences of the αAmy3and the 20-bp sequence of the Shrunken promoters. However, the TATCCA element is present between position −136 and position −141 of the Shrunken promoter, which could be another control element that exhibits a function similar to the 20-bp sequence (Maas et al., 1990).


Information concerning the sugar status of plant cells is of great importance in initiating changes in gene expression and subsequent metabolic and developmental responses. The mechanisms used by plant cells to sense sugars and to process this information are largely unknown. Yeast has been an essential model for studies on the mechanisms of sugar sensing and signal transduction employed in plant cells. In yeast, genes required for growth on carbon sources other than Glc are repressed by the presence of Glc in the medium and can be derepressed when Glc is removed. This is the phenomenon of Glc repression that requires a mechanism for sensing the availability of Glc. Hexokinase, the enzyme that catalyzes the phosphorylation of hexose sugars at the first step of the glycolytic pathway, has been implicated as a Glc sensor in organisms as diverse as yeast (Rose et al., 1991) and mammals (Efrat et al., 1994). Recent studies suggest that hexokinase also acts as a primary sugar sensor in plants (Jang and Sheen, 1997; Smeekens and Rook, 1997). However, the notion that hexokinase is a primary sugar sensor was recently challenged, and multiple sugar-sensing pathways were proposed to exist in plants (Halford et al., 1999). The other sugar-sensing systems proposed to exist in plants are a hexose transporter and/or receptor signaling pathway and a Suc transporter and/or receptor signaling pathway (Smeekens and Rook, 1997; Halford et al., 1999).

Knowledge of the downstream components of the Glc-signaling pathway in plants has just begun to emerge. In fungi, the SNF1 protein (Suc non-fermenting 1) is required for derepression of nearly all Glc-repressed genes and is an integral component of the sugar signal transduction pathway (Ronne, 1995). SNF1 is a Ser/Thr protein kinase and the active kinase is a high-molecular-mass complex. The SNF1 complex contains three proteins that are homologs of three subunits of the mammalian AMPK (AMP-activated protein kinase) (Hardie et al., 1998). AMPK is one component of a kinase cascade that is activated in a highly sensitive manner by the elevation of AMP and the depletion of ATP. The AMPK cascade has been shown to be activated by environmental stresses that deplete cellular ATP, for example, in pancreatic β cells by Glc deprivation (Salt et al., 1998). It is therefore suggested that the SNF1 complex in yeast might be activated in a manner similar to AMPK in mammals in response to Glc deprivation, and a change in the ATP level might be the signal that indicates the availability of sugar (Halford et al., 1999).

Recently, the requirement for a SNF1-related protein kinase-1 (SnRK1) in Suc-activated expression of a Suc synthase gene was demonstrated in potato by an antisense RNA approach (Purcell et al., 1998). This study indicated that SNF1 in plants may play a role analogous to that of SNF1 in yeast (Halford et al., 1999). However, whether SnRK1 activity is regulated by Glc or another hexose and whether plant SNF1 homologs also play a role in the derepression of sugar-repressible genes remains to be determined. Identification of other functional components in the sugar signal transduction pathway are also important for determining whether the mechanisms through which cells sense sugar availability and respond by changing gene expression are conserved or diverged between yeast and plants throughout evolution. Based on the available information, a model of sugar sensing, signal transduction, and mechanisms of gene regulation in plant cells is shown in Figure3.

Fig. 3.

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Hypothetical model of genetic and cellular responses of plant cells to sugar, including a sugar signal transduction pathway and a mechanism of gene regulation. Three elements function as sugar sensors: a hexokinase, a sugar transporter, and a change in the AMP/ATP ratio. Protein phosphatase and protein kinase are involved in the signal transduction pathway. In some cases, the SNF1 complex may be a component of the signal transduction pathway. The expression level of sugar-regulated genes is determined by the control of promoter transcriptional activity and mRNA stability. In the presence of sugar, the expression of sugar-starvation-induced genes is suppressed and there is no change in metabolism or vacuolar autophagic activity. Under sugar starvation, an opposite action of these events likely occurs.


Bacteria and yeast have developed mechanisms to react to depletion of nutrients in their environment and protect themselves against damage caused by nutrient stress and other stresses. Some components of stress signal pathways have been shown to be conserved among yeast, mammal, and plant cells (Ruis and Schüller, 1995; Hardie et al., 1998). Studies on the mechanisms of signal transduction and gene regulation in response to sugar deprivation will determine which strategies nature uses to deal with problems encountered by cells living in an unfavorable environment. However, many questions with respect to the underlying molecular mechanisms employed by plants in the adaptation to sugar deprivation remain to be answered. An understanding of how plants respond to sugar starvation and regulate the mobilization of stored carbohydrates can also help us to design crops with higher stress-tolerant capacity and is thus of biotechnological importance.

Sugar Supplement for HydroponicsSugar Supplement for Hydroponics
Most growers feed their plants with sugar without understanding its importance. For instance, the bouquet you gift your loved one on Valentine’s Day are generally kept in water with sugar to extend their bloom. By simply adding fulvic acid and humic acidto your nutrient solution will automatically provide build blocks for sugar. Very few growers know that there is a meter called Brix Meter which is available in the market to measure sugar levels in the leaves. The more sugar you provide your plants the healthier they are and it also improves overall hydroponics yield.Plants in general are photoautotrophs; this means plants can synthesize their food directly with the help of light and inorganic compounds using photons. Plants do this using a process called photosynthesis. Carbon dioxide and water are the inorganic compounds and sunlight is the energy source. The final product consists of a simple sugar, glucose and oxygen.The chemical reaction formed is:6CO2 + 12H2O + photons -> C6H2O6 + 6O2 + 6H2O

(gas)       (liquid)                     (aqueous)  (gas)   (liquid)

The process called carbon fixation uses a high-energy molecule, ATP, to create sugar. Glucose is simple sugar produced from carbon fixation. These simple sugar produced called glucose, also known as monosaccharide can be easily broken down by plants and are used for energy. Cellulose is categorized as complex sugar or polysaccharides are also produced during the process. Cellulose or polysaccharides have a chain of two or more types of sugar and are used for lipid and amino acid biosynthesis. In cellular respiration polysaccharide is used as fuel and is the prime component of all green plants cell walls.

With proper knowledge and understanding of photosynthesis, you’ll know the importance of sugar produced through this process. You’ll know that sugar and starch are very important for the plants as they help to maintain plants’ metabolism rate. Sugar helps in forming building blocks that keep the plants cells together. It’s clear that your plants have sweet-tooth and are good at making the sugar they need.

Flowering plants burn carbohydrates to successfully produce bigger vegetables and fruits during bloom phase. The whole process of photosynthesis takes up a lot of energy.  By adding organic carbohydrate supplement into your nutrient solution the allocated carbohydrates will be replenished easily. Therefore, this will save energy that your plants utilize to create sugar and instead use it for flowering process.

Many beneficial bacteria and fungi break down sugar and for this they use energy which otherwise should have been used for other purposes. Remember, the more the number of beneficial microorganisms the easier is the absorption of nutrients by the roots. This promotes improved flowering and healthy looking plants.

It’s advisable to provide your plants with something organic to improve the taste and aroma of the fruits and vegetables of your plants. Xylose and arabinose are also types of natural sugar essential for your plants.

For any sugar supplement, glucose should be the main ingredient. It’s an excellent source for producing proteins and in lipid metabolism. Fructose is also one important component of most fruits, berries and melons. It’s twice as sweets as disaccharide sucrose (combination of glucose and fructose). Disaccharide maltose is also one important sugar because the enzymes can break it into two glucose molecules.

These are important types of sugar produced by plants naturally. An ideal supplement should contain these simple and complex sugar substances along with nutrient solution. This will encourage plants to increase the level of sugar and also let your plants use the available energy in other important productive areas. Your fruits and vegetables will be tastier and aromatic as well.

Sugar-transport proteins play a crucial role in the cell-to-cell and long-distance distribution of sugars throughout the plant. In the past decade, genes encoding sugar transporters (or carriers) have been identified, functionally expressed in heterologous systems, and studied with respect to their spatial and temporal expression. Higher plants possess two distinct families of sugar carriers: the disaccharide transporters that primarily catalyse sucrose transport and the monosaccharide transporters that mediate the transport of a variable range of monosaccharides. The tissue and cellular expression pattern of the respective genes indicates their specific and sometimes unique physiological tasks. Some play a purely nutritional role and supply sugars to cells for growth and development, whereas others are involved in generating osmotic gradients required to drive mass flow or movement. Intriguingly, some carriers might be involved in signalling. Various levels of control regulate these sugar transporters during plant development and when the normal environment is perturbed. This article focuses on members of the monosaccharide transporter and disaccharide transporter families, providing details about their structure, function and regulation. The tissue and cellular distribution of these sugar transporters suggests that they have interesting physiological roles.

In addition to their essential roles as substrates in carbon and energy metabolism and in polymer biosynthesis, sugars have important hormone-like functions as primary messengers in signal transduction. The pivotal role of sugars as signaling molecules is well illustrated by the variety of sugar sensing and signaling mechanisms discovered in free-living microorganisms such as bacteria and yeast (Stulke and Hillen, 1999Go; Rolland et al., 2001Go). For such unicellular organisms, nutrient availability is the main extracellular factor controlling growth and metabolism. The role of nutrients as regulatory molecules has come to be appreciated only recently in mammals despite extensive previous research on Glc homeostasis and diabetes (Hanson, 2000Go; Rolland et al., 2001Go).

In plants, sugar production through photosynthesis is a vital process, and sugar status modulates and coordinates internal regulators and environmental cues that govern growth and development (Koch, 1996Go; Sheen et al., 1999Go; Smeekens, 2000Go). Although the regulatory effect of sugars on photosynthetic activity and plant metabolism has long been recognized, the concept of sugars as central signaling molecules is relatively novel. Recent progress has begun to reveal the molecular mechanisms underlying sugar sensing and signaling in plants, including the demonstration of hexokinase (HXK) as a Glc sensor that modulates gene expression and multiple plant hormone-signaling pathways (Sheen et al., 1999Go; Smeekens, 2000Go). Analyses of HXK mutants will provide new evidence for distinct signaling and metabolic activities. Diverse roles of Snf1-related protein kinases (SnRKs) in carbon metabolism and sugar signaling also are emerging (Halford and Hardie, 1998Go; Hardie et al., 1998Go). In addition, Suc, trehalose, and other HXK-independent sugar sensing and signaling pathways add more complexity in plants (Goddijn and Smeekens, 1998Go; Lalonde et al., 1999Go; Smeekens, 2000Go).

Biochemical, molecular, and genetic experiments have supported a central role of sugars in the control of plant metabolism, growth, and development and have revealed interactions that integrate light, stress, and hormone signaling (Roitsch, 1999Go; Sheen et al., 1999Go; Smeekens, 2000Go; Gazzarrini and McCourt, 2001Go; Finkelstein and Gibson, 2002Go) and coordinate carbon and nitrogen metabolism (Stitt and Krapp, 1999Go; Coruzzi and Bush, 2001Go; Coruzzi and Zhou, 2001Go). A number of reviews have appeared in the past few years emphasizing different aspects of sugar signaling and its interactions with other plant signal transduction pathways. In this review, the extent and impact of the sugar signaling network on plant life is illustrated. We explore diverse sugar responses, summarize biochemical and genetic evidence for different sugar sensing and signaling mechanisms, consider the extensive regulatory web that mediates sugar and hormone signaling, and suggest possible directions for future research.


Photosynthesis is active primarily in mature leaf mesophyll cells, and photosynthate is transported, primarily as Suc, to meristems and developing organs such as growing young leaves, roots, flowers, fruit, and seed. Light and sugars regulate these growth activities by a coordinated modulation of gene expression and enzyme activities in both carbohydrate-exporting (source) and carbohydrate-importing (sink) tissues (Figure 1) . This ensures optimal synthesis and use of carbon and energy resources and allows for the adaptation of carbon metabolism to changing environmental conditions and to the availability of other nutrients (Stitt and Krapp, 1999Go; Coruzzi and Bush, 2001Go; Coruzzi and Zhou, 2001Go; Grossman and Takahashi, 2001Go). In general, low sugar status enhances photosynthesis, reserve mobilization, and export, whereas the abundant presence of sugars promotes growth and carbohydrate storage (Figure 1) (Koch, 1996Go). The circadian clock can play an important role in carbon partitioning and allocation (Harmer et al., 2000Go). Several photosynthetic genes, for example, peak in expression near the middle of the day, whereas a number of genes involved in sugar consumption, transport, and storage peak near the end of the day. During the night, genes involved in starch mobilization reach their highest expression levels (Harmer et al., 2000Go). However, although the circadian clock may allow plants to “anticipate” daily changes, the actual sensing of the quality and quantity of light and especially sugars (as the end products of photosynthesis) ensures an appropriate “response” of metabolism to specific situations. For example, variations in the environment can decrease photosynthetic efficiency and result in sugar-limited conditions in parts of the plant, which downregulate biosynthetic activity to conserve energy and protect cells against nutrient stress while upregulating starch degradation and protein and lipid catabolism to sustain respiration and metabolic activity (Yu, 1999Go; Fujiki et al., 2000Go). Photosynthetic acclimation to increased CO2 is likely the result of sugar repression, especially under nitrogen deficiency, and sugar repression of photosynthetic gene expression, chlorophyll accumulation, and seedling development can be antagonized by nitrate signals (Moore et al., 1999Go; Stitt and Krapp, 1999Go). Moreover, several N-regulated genes are coregulated by sugars (Wang et al., 2000Go; Wang et al., 2001Go; Coruzzi and Bush, 2001Go; Coruzzi and Zhou, 2001Go). In oxygen-limited environments (e.g., in flooded root systems), plant cells can shift metabolism to fermentation to sustain glycolysis by direct NAD+ regeneration (Tadege et al., 1999Go), and interference between sugar and oxygen signals has been shown (Koch et al., 2000Go). Thus, plants can display photosynthesis, respiration, and fermentation at the same time in different tissues through a complex regulatory system that involves sugar signaling and integrates different metabolic, developmental, and environmental signals to control metabolic mode and activity.

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Figure 1. Differential Effects of Sugars on Plant Source and Sink Activities.Suc is transported from photosynthesizing source leaves to sink organs such as roots, meristems, young leaves, flowers, fruit, and developing seed. Lowered (L) sugar levels can increase source activities, including photosynthesis, nutrient mobilization, and export. In contrast, higher (H) sugar levels in sink tissues stimulate growth and storage. Accumulation of higher (H) sugar levels in source tissues, however, is believed to downregulate photosynthesis, ensuring the maintenance of sugar homeostasis. The differential source-sink effects allow the adaptation of carbon metabolism to changing environmental conditions and to the availability of other nutrients.

Growth and Development
The effect of carbon allocation on organ and whole plant architecture is illustrated most dramatically by carbohydrate storage and the concomitant cell expansion in reserve organs such as roots, fruit, seed, and tubers. However, cell division and differentiation can be ascribed to both changes in metabolic activity and sophisticated developmental switches (Jackson, 1999Go; Wobus and Weber, 1999aGo; Hajirezaei et al., 2000Go; White et al., 2000Go; Giovannoni, 2001Go). In Vicia faba embryos, gradients of sugars have been reported to correlate spatially with mitotic activity (Borisjuk et al., 1998Go). Consistently, Arabidopsis D-type cyclin gene expression is regulated differentially by sugars (Riou-Khamlichi et al., 2000Go). Therefore, sugars also could act as morphogens, providing positional information to the cell cycle machinery and different developmental programs. Remarkably, differential display analysis using portions of tomato meristems destined to form leaves revealed spatially regulated carbohydrate metabolism within the meristem and suggested the involvement of carbohydrate metabolism in organogenesis (Pien et al., 2001Go).

Sugar sensing and signaling are involved in the control of growth and development during the entire plant life cycle. During germination and early seedling development, sugars can repress nutrient mobilization, hypocotyl elongation, cotyledon greening and expansion, and shoot development (Yu et al., 1996Go; Dijkwel et al., 1997Go; Jang and Sheen, 1997Go; Perata et al., 1997Go; Kurata and Yamamoto, 1998Go; Arenas-Huertero et al., 2000Go; Gibson, 2000Go; Smeekens, 2000Go; Eastmond and Graham, 2001Go; Gazzarrini and McCourt, 2001Go). High sugar accumulation during early seedling development may reflect undesirable growth conditions at a crucial developmental period (Lopez-Molina et al., 2001Go), resulting in a reversible developmental arrest that acts as a protection mechanism. Sugar-dependent seedling phenotypes have been used extensively for the selection of sugar signaling mutants in Arabidopsis, including both sugar-insensitive and sugar-hypersensitive mutants (Table 1).

Based on a growth response in which a high level of Glc blocks the switch to postgermination development in Arabidopsis, both Glc-insensitive (gin) and Glc-oversensitive (glo) mutants have been isolated. Table 2 provides a list of gin mutants identified using the same genetic screen. Genetic analyses showed that multiple alleles of the gin1, gin2, gin3, gin4, gin5, and gin6 mutants have been obtained (Table 2). Each gin mutant has been mapped to a different site on four chromosomes (Table 2). Some of the gin mutants are allelic to other sugar, abscisic acid (ABA), and salt mutants (Sheen et al., 1999Go; Gibson, 2000Go; Smeekens, 2000Go; Rook et al., 2001Go; W.-H. Cheng and J. Sheen, unpublished data; P.L. Rodríguez, personal communication) based on phenotype comparison, chromosomal location, and allelism tests (Table 2) (Zhou et al., 1998Go; Arenas-Huertero et al., 2000Go; W.-H. Cheng and J. Sheen, unpublished data; L. Zhou and J. Sheen, unpublished data).

The effects of sugars on floral transition have been studied in more detail recently and appear to be very complex. In Arabidopsis, increased leaf carbohydrate export and starch mobilization are required for flowering, suggesting that phloem carbohydrates have a critical function in floral transition (Corbesier et al., 1998Go). Interestingly, the addition of Suc can rescue the late-flowering phenotype of several mutants (Araki and Komeda, 1993Go; Roldan et al., 1999Go) and even promotes leaf morphogenesis and flowering in the dark (Roldan et al., 1999Go). However, high exogenous concentrations of sugars have been shown to delay flowering significantly (Zhou et al., 1998Go). A recent report confirmed the pleiotropic effects of sugars on floral transition, depending on sugar concentration, vegetative growth phase, and genetic background. Sugars may control floral transition by positively and negatively regulating the expression of floral identity genes (Ohto et al., 2001Go).

Sugar sensing and signaling also are implicated in the regulation of leaf senescence that coincides with a decline in chlorophyll content and photosynthetic activity (Jiang et al., 1993Go; Bleeker and Patterson, 1997Go; Quirino et al., 2000Go). Sugars are known to repress photosynthetic gene expression, and in transgenic plants, HXK expression correlates well with the rate of leaf senescence (Dai et al., 1999Go; Xiao et al., 2000Go). Interestingly, the expression of phospholipase D, which is important for leaf senescence (Fan et al., 1997Go), is induced by Glc (Xiao et al., 2000Go). Leaf contents of Glc and Fru were shown to increase with leaf age, whereas starch content decreased (Wingler et al., 1998Go; Quirino et al., 2001Go), and the monosaccharide transporter homolog SFP1 was induced during advanced leaf senescence (Quirino et al., 2001Go). However, although exogenously supplied sugars induce expression of the senescence-associated gene SAG21 in a HXK-dependent manner (Xiao et al., 2000Go), another well-characterized senescence marker, SAG12, is repressed by sugars in senescing Arabidopsis leaves (Noh and Amasino, 1999Go). The regulation of different SAGs may be controlled differentially by other factors besides sugars, such as developmental state and hormones (He et al., 2001Go).

The recent demonstration of glucose oversensitive phenotypes of the Arabidopsis hys1/cpr5 mutants, selected based on leaf hypersenescence and constitutive expression of pathogenesis-related genes, also suggests a role for sugar signaling in senescence and defense (Yoshida et al., 2002Go).

Abiotic and biotic stress stimuli, such as drought, salinity, wounding, and infection by viruses, bacteria, and fungi, can modulate source-sink activities. Because extracellular invertase, a key enzyme for hydrolyzing Suc (Sturm, 1999Go), is regulated by stress stimuli and hormones, it has been proposed to be a central modulator of assimilate partitioning, integrating sugar, stress, and hormone signals (Roitsch, 1999Go). Although stress may alter sugar levels, experiments with protein kinase (PK) inhibitors suggest that sugars and stress-related stimuli also may activate different signaling pathways independently (Ehness et al., 1997Go; Roitsch, 1999Go). It is intriguing that sugars regulate the expression of wound-inducible proteinase inhibitor II and lipoxygenase genes (Johnson and Ryan, 1990Go; Sadka et al., 1994Go), pathogenesis-related (PR) genes (Herbers et al., 1996Go; Xiao et al., 2000Go), and dark-inducible (DIN) genes (Fujiki et al., 2001Go). Some of the DIN genes also are activated by sugar starvation, pathogens, and senescence (Quirino et al., 2000Go; Fujiki et al., 2001Go; Ho et al., 2001Go), suggesting that a response to metabolic stress could be the underlying mechanism.

In addition, many jasmonate-, ABA-, and stress-inducible genes are coregulated by sugars (Reinbothe et al., 1994Go; Sadka et al., 1994Go). Further studies will be required to reveal the genetic and molecular basis of sensing and signaling pathways connecting sugar and stress in plants. Interestingly, an ancient regulatory system controlling metabolism, stress resistance, and aging appears to be conserved from yeast to mice (Kenyon, 2001Go). Both caloric restriction and increased oxidative stress resistance are able to increase life span. In yeast, Glc sensing and signaling pathways play a central role in longevity (Ashrafi et al., 2000Go; Lin et al., 2000Go; Fabrizio et al., 2001Go). The delayed senescence and increased stress resistance observed in Arabidopsis HXK antisense plants (Xiao et al., 2000Go) similarly connect plant sugar metabolism and sensing with the control of stress resistance and aging. Two Arabidopsis proteins, ZAT10 and AZF2, with similarities to the yeast zinc-finger transcription factors Msn2 and Msn4 have been isolated in a yeast (snf4Δ) suppressor screen (Kleinow et al., 2000Go). In yeast, Msn2 and Msn4 control growth-inhibitory genes (Smith et al., 1998Go). They are regulated positively by stress and negatively by Glc through phosphorylation and cytosolic translocation (Gorner et al., 1998Go). Whether these factors are involved in Glc regulation in plants awaits further functional analysis.

Gene Expression
Research in plant sugar signaling has been focused largely on gene expression. A wide variety of genes are sugar regulated at the transcriptional level, including genes involved in photosynthesis, carbon and nitrogen metabolism, stress responses, and secondary metabolism in different plant species. However, little is known about the actual transcriptional machinery underlying these responses. Detailed analysis of different maize photosynthetic gene promoters did not reveal common regulatory elements for sugar regulation, suggesting the involvement of diverse transcription factors (Sheen, 1990Go, 1999Go). Examination of Glc-repressed rice α-amylase gene promoters has identified several cis elements required for sugar-regulated gene expression (Chan and Yu, 1998bGo; Hwang et al., 1998Go; Lu et al., 1998Go; Morita et al., 1998Go) and mRNA stability (Chan and Yu, 1998aGo). Specific regulatory elements involved in Glc repression also have been identified in the promotors of the cucumber malate synthase (Sarah et al., 1996Go) and bean RBCS2 (Urwin and Jenkins, 1997Go) genes.

Currently, most progress has been made through the functional dissection of sugar-induced gene promoters. Suc-responsive elements are found in the patatin class I promoter. Similar SP8 motifs are present in the promoters of the sweet potato sporamin and {beta}-amylase genes, and interact with nuclear factors (Liu et al., 1990Go; Ishiguro and Nakamura, 1992Go, 1994Go; Grierson et al., 1994Go; Kim et al., 1994Go). Similar Suc-responsive sequences also are found in several Suc-inducible Suc synthase genes (Fu et al., 1995Go). A gene encoding a DNA binding protein that recognizes the SP8 motif in the sweet potato sporamin and potato {beta}-amylase gene promoters, SPF1, has been cloned. It encodes a negative regulator that is repressed transcriptionally by Suc (Ishiguro and Nakamura, 1994Go). SPF1 has putative homologs in cucumber (Kim et al., 1997Go) and Arabidopsis that encode a WRKY domain transcription factor. The (T)TG-AC(C/T) core sequence of WRKY binding elements (W-box) is found in the promoters of the wheat, barley, and wild oat α-AMY2 gene (Rushton et al., 1995Go). W-boxes also are found in the promoters of an α-amylase gene homolog and many Arabidopsis genes possibly involved in plant defense (Du and Chen, 2000Go; Maleck et al., 2000Go).

Other motifs frequently found in several sugar-regulated promoters are the G-box and related sequences. The G-box motif (CACGTG) is involved in the transcriptional control of a variety of stimuli, such as phytochrome-mediated control of gene expression through binding of the PIF3 (Martinez-Garcia et al., 2000Go) and HY5 (Chattopadhyay et al., 1998Go) transcription factors. In addition, this motif is very similar to the CCACGTGG ABA-responsive element (Pla et al., 1993Go). Interestingly, {beta}-amylase transcript is induced by ABA (Ohto et al., 1992Go), and induction of the {beta}-phaseolin promoter by exogenous ABA in tobacco embryos is modulated by external Suc (Bustos et al., 1998Go). These data suggest that sugar, light, hormone, and defense signaling may converge in the transcriptional control of W- and G-boxes in diverse promoters. More thorough analysis is required to reveal the precise molecular basis of these interactions. The recent discovery of new sugar-responsive elements (Maeo et al., 2001Go) may stimulate the identification of specific transcription factors in sugar signaling.

As shown for the regulation of rice α-amylase transcript, sugars can repress gene expression by affecting mRNA stability through specific 3′ untranslated region sequences (Chan and Yu, 1998aGo). Also for the transcripts encoding rice ADH2 (alcohol dehydrogenase 2), G3PD (glyceraldehyde-3-phosphate dehydrogenase), and SSP2 (Suc synthase phosphate 2), sugars can enhance their stability (Ho et al., 2001Go). Other striking examples are the differential RNA processing and translation of the maize cell wall invertase transcripts mediated by 3′ untranslated region sequences (Cheng et al., 1999Go) and the 5′ untranslated region–dependent repression of translation of the Arabidopsis ATB2 mRNA, encoding a bZIP transcription factor, by sugars (Rook et al., 1998Go).


Sugar Signals
Sugar control of metabolism, growth and development, stress, and gene expression has long been thought to be a metabolic effect. However, the control of gene expression observed with nonmetabolizable or partially metabolizable hexoses or hexose and Suc analogs clearly suggest the involvement of specific signal sensing and transduction mechanisms that do not require sugar catabolism (Figure 2) (Krapp et al., 1993Go; Graham et al., 1994Go; Jang and Sheen, 1994Go; Martin et al., 1997Go; Klein and Stitt, 1998Go; Roitsch, 1999Go; Sheen et al., 1999Go; Loreti et al., 2000Go; Smeekens, 2000Go; Brouquisse et al., 2001Go; Fernie et al., 2001Go). To study diverse sugar responses, sugars and sugar analogs have been applied exogenously to whole seedlings or plants, detached organs or tissues, and protoplasts or suspension-cultured cells. Manipulation of sugars in planta also has been accomplished by direct injection, petiole girdling, increasing CO2, altering light intensity, or the genetic manipulation of invertase genes (von Schaewen et al., 1990Go; Sonnewald et al., 1991Go; Moore et al., 1999Go; Stitt and Krapp, 1999Go; Sturm and Tang, 1999Go; Tang et al., 1999Go; Pego et al., 2000Go).

Possible Sugar Signals and Sensing Sites in Plant Cells.Glc (and Fru) can be transported into the cell by hexose transporters or mobilized from cytosolic and vacuolar Suc and plastid starch. Glc then enters metabolism after HXK-catalyzed phosphorylation. The HXK sugar sensor, as a cytosolic protein or associated with mitochondria or other organelles (see text), then could activate a signaling cascade through HXK-interacting proteins (HIPs) or affect transcription directly after nuclear translocation. Possibly, different HXK (and fructokinase [FRK]) isoforms and HXK-like proteins have distinct metabolic and signaling functions. Metabolic intermediates could trigger signal transduction by activating metabolite sensors (S). Negative regulation of SnRK activity by Glc-6-phosphate, for example, suggests that SnRKs might act as sensors of metabolic activity. Finally, sugars, including Suc and hexoses and nonmetabolizable sugars and sugar analogs, also could be sensed at the plasma membrane by sugar transporters or transporter-like proteins or by specific sugar receptors (R). Solid lines represent transport and enzymatic reactions involved in sugar sensing and signaling, and dashed lines represent putative interactions and translocations. ER, endoplasmic reticulum.

Although hexoses are potent signals sensed in plants, Suc-specific (Chiou and Bush, 1998Go; Rook et al., 1998Go) and trehalose-mediated (Goddijn and Smeekens, 1998Go) signaling pathways also play important roles in regulating development and gene expression. In developing seed, it has been suggested that Suc regulates differentiation and storage, whereas hexoses control growth and metabolism (Weber et al., 1997Go; Wobus and Weber, 1999bGo). The ability of both 3-O-methylglucose and 6-deoxyglucose to regulate gene expression indicates the presence of HXK-independent pathways through novel sensors in plants (Martin et al., 1997Go; Roitsch, 1999Go). Recently, new sugar sensing mechanisms also have been revealed through the use of disaccharide analogs (palatinose and turanose) that are not even membrane permeable (Loreti et al., 2000Go; Fernie et al., 2001Go).

Sugar Sensing Mechanisms
To activate signal transduction pathways, sugars first have to be sensed. The sugar’s dual function as a nutrient and a signaling molecule, however, significantly complicates analysis of the mechanisms involved (Rolland et al., 2001Go). Even in yeast in which downstream components of sugar signaling pathways have been characterized in detail, elucidation of the initial Glc sensing and activation mechanisms has been difficult. Only recently, the involvement of transporter-like Glc sensors (Snf3 and Rgt2) and a G protein–coupled receptor (Gpr1) and new evidence for Hxk2 function in Glc signaling have been reported (Johnston, 1999Go; Rolland et al., 2001Go). It has been proposed that similar transporter-like Glc sensors and receptors could function in yeast, mammals, and plants (Lalonde et al., 1999Go; Barker et al., 2000Go; Williams et al., 2000Go; Rolland et al., 2001Go). Interestingly, mammalian sweet taste receptors are encoded by GPR genes and can distinguish Suc from Glc (Nelson et al., 2001Go). Despite initial concerns, compelling evidence indicates that HXK also functions as a sugar sensor in plants (Moore and Sheen, 1999Go).

A regulatory role for HXK in plant hexose sensing was suggested by testing the effects of a variety of sugars, Glc analogs, and metabolic intermediates on photosynthesis and glyoxylate cycle gene repression in Chenopodium (Krapp et al., 1993Go) and cucumber (Graham et al., 1994Go) cell cultures and in a maize protoplast transient expression system (Jang and Sheen, 1994Go). Sugars that are substrates of HXK, including Man and 2-deoxyglucose, which are phosphorylated but inhibit Glc-6-phosphate and ATP production (Klein and Stitt, 1998Go), cause repression of photosynthetic gene expression at low physiological levels (1 to 10 mM in maize mesophyll protoplasts) (Jang and Sheen, 1994Go). The repression is blocked by the HXK-specific competitive inhibitor mannoheptulose (Jang and Sheen, 1994Go). L-Glc (not transported), 6-deoxyglucose and 3-O-methylglucose (transported but not phosphorylated), and sugar phosphates (delivered into the protoplasts by electroporation) do not trigger the same repression. Possible depletion of Pi and ATP as a cause of reduced gene expression has been excluded by the inability of Pi and ATP to relieve repression (Graham et al., 1994Go; Jang and Sheen, 1994Go). Consistently, 2-deoxyglucose and Man can arrest seed germination by a mechanism that affects sugar signaling independently of hexose metabolism or depletion of seed ATP and Pi levels. Mannoheptulose also overcomes this inhibition (Pego et al., 1999Go). Glc repression of the α-amylase gene in rice embryos (Umemura et al., 1998Go) and Arabidopsis DIN genes is likely mediated by HXK (Fujiki et al., 2000Go). It is clear that caution must be taken when poorly or nonmetabolizable sugar analogs such as Man, 2-deoxyglucose, and 3-O-methylglucose are used, because they often produce toxic side effects and eventually can result in cell death (Stein and Hansen, 1999Go; Brouquisse et al., 2001Go).

Experiments with transgenic Arabidopsis plants further indicate the uncoupling of HXK catalytic and regulatory functions (Jang et al., 1997Go). Overexpression of the sense and antisense AtHXK1 or AtHXK2 gene results in sugar hypersensitivity or hyposensitivity, respectively, as demonstrated by altered sugar responses in seedling development and gene expression. On the contrary, overexpression of the yeast HXK2 gene reduces sugar sensitivity in transgenic plants despite a marked increase in kinase activity (Jang et al., 1997Go). Definitive proof for the dual function of HXK obviously must come from mutant analysis. In yeast, Hxk2 is implicated in the Glc repression of genes involved in the respiration and metabolism of alternative carbon sources (Rolland et al., 2001Go). Mutations that uncouple HXK’s signaling function from its catalytic activity have been isolated (Hohmann et al., 1999Go; Kraakman et al., 1999Go; Mayordomo and Sanz, 2001aGo). However, the most striking example of such a dual function for a sugar kinase comes from the Gal induction pathway in yeast. Gene expression involved in Gal metabolism is controlled by the transcriptional activator Gal4, which is associated with and inhibited by the Gal80 repressor. In the presence of Gal and ATP, galactokinase (Gal1) or its catalytically inactive homolog Gal3 binds to Gal80, thereby destabilizing the Gal4-Gal80 complex and enabling transcription by Gal4 (Bhat et al., 1990Go; Zenke et al., 1996Go; Sil et al., 1999Go).

In the Arabidopsis genome, there are six HXK and HXK-like (HXKL) genes (Arabidopsis Genome Initiative, 2000Go), three fructokinase (FRK) genes, and several FRK-like genes (Arabidopsis Genome Initiative, 2000Go; Pego and Smeekens, 2000Go). Mutational and functional analyses of Arabidopsis HXKs and HXKLs suggest their involvement in sugar sensing and signaling (B. Moore and J. Sheen, unpublished data). Importantly, two null mutants of AtHXK1 (gin2-1 and gin2-2) have been isolated and show Glc insensitivity in gene expression and development (Figure 3) . The isolation of AtHXK1 mutants with distinct catalytic and regulatory activity would provide invaluable tools to elucidate broad sugar responses at the cellular and whole plant levels. In tomato, transcripts of both FRK1 and FRK2 are induced by exogenous application of Glc, Fru, and Suc (Kanayama et al., 1998Go). Although it is generally believed that FRKs serve important metabolic functions, the identification of an frk2 null mutation in a Man-insensitive mig mutant (Pego and Smeekens, 2000Go) suggests that FRK also may be involved in sugar sensing.

Mutant Phenotype and Complementation by 35:: AtHXK1.Plants were grown on 6% Glc Murashige and Skoog (1962)Go medium for 5 days under light. WT, wild type.

HXK sensing and signaling function likely are dependent on HXK’s subcellular localization, translocation, and/or interactions with downstream effectors. A model summarizing possible sugar sensing sites in plant cells is presented in Figure 2. Yeast Hxk2, for example, has been shown to interact with the protein phosphatase (PP) complex that modifies Snf1 kinase activity, thereby stimulating Glc repression (Alms et al., 1999Go; Sanz et al., 2000Go). Yeast Hxk2 also is found in the nucleus, participating directly in regulatory DNA-protein complexes with cis-acting regulatory elements of a Glc-repressed gene (Herrero et al., 1998Go; Randez-Gil et al., 1998Go). Mammalian HXK activity is known to be regulated by protein interactions that ensure proper subcellular localization and function. Mammalian HXKI, for example, is bound to the outer mitochondrial membrane, which enables direct access to the ATP generated by oxidative phosphorylation (Adams et al., 1991Go; BeltrandelRio and Wilson, 1992aGo, 1992bGo). In hepatocytes and pancreatic {beta}-cells, glucokinase (HXKIV)-interacting proteins control sugar-regulated nucleocytoplasmic glucokinase translocation and activity (Van Schaftingen et al., 1994Go; Farrelly et al., 1999Go; Munoz-Alonso et al., 2000Go; Shiraishi et al., 2001Go). Interestingly, human pancreatic glucokinase complements the Glc signaling defects of yeast hxk2 mutants (Mayordomo and Sanz, 2001bGo).

In plants, HXK has long been considered a cytosolic protein involved in glycolysis (Plaxton, 1996Go). However, the occurrence of noncytosolic, organelle-associated HXK has been demonstrated (Borchert et al., 1993Go; Galina et al., 1995Go; Wiese et al., 1999Go). In maize roots, most of the noncytosolic HXK is bound to mitochondria (Galina et al., 1995Go, 1999Go), whereas a substantial portion appears to be associated with the Golgi apparatus and other cellular membranes (da-Silva et al., 2001Go). Possibly, HXK is involved directly in UDP-Glc synthesis and Golgi glycosylation (Galina and da-Silva, 2000Go; da-Silva et al., 2001Go). A substantial fraction of spinach leaf HXK1 is located at the outer envelope membrane of plastids via its N-terminal membrane anchor (Wiese et al., 1999Go).

HXK associated with chloroplasts and plastids from nongreen tissues could be involved in the direct phosphorylation of Glc when it leaves the organelles as a product of starch hydrolysis (Focks and Benning, 1998Go; Wiese et al., 1999Go). However, in maize, the ADP inhibition of noncytosolic HXK isoforms suggests that these HXKs may not be involved in glycolysis and thus could play a regulatory role in sugar sensing (da-Silva et al., 2001Go). Induction of systemic acquired resistance and repression of photosynthetic gene expression in transgenic tobacco plants expressing yeast-derived invertase in the apoplast or vacuole suggest that hexose sensing somehow may involve the secretory pathway (Herbers et al., 1996Go). In Arabidopsis, HXK1 is found associated with mitochondria (B. Moore and J. Sheen, unpublished data), but the physiological and biochemical function of this interaction remains to be elucidated.

Sugar Metabolites
Because sugars are nutrients and metabolized extensively, their presence also could be sensed through downstream metabolites. Sugar induction of PR1 and PR5, for example, appears to depend on HXK catalytic activity but not on its signaling function, suggesting the involvement of one or more catabolites (Xiao et al., 2000Go). The identification of Glc-6-phosphate as a regulator of SnRK activity provides a possible mechanism underlying some Glc responses in plants (Toroser et al., 2000Go). Acetate and other respiratory intermediates have been shown to affect gene expression (Sheen, 1990Go; Koch, 1996Go; Koch et al., 2000Go), possibly indirectly through pH effects. In addition, changes in energy status also can affect gene expression and enzyme activities. In mammals, for example, high ATP levels generated by Glc catabolism in pancreatic {beta}-cells are known to activate ATP-sensitive K+ channels and eventually stimulate insulin release (Matschinsky et al., 1998Go). Glc depletion, on the other hand, causes a high AMP/ATP ratio and can activate AMP-dependent protein kinases (Hardie et al., 1998Go).

The disaccharide trehalose has been shown to affect plant metabolism and development. The presence of trehalose as an endogenous compound has long been thought to be confined to resurrection plants, in which it serves as a stress protectant, but the Arabidopsis genome sequence and yeast mutant complementation have revealed the presence of functional plant genes encoding enzymes involved in trehalose synthesis and hydrolysis (Goddijn and Smeekens, 1998Go; Goddijn and van Dun, 1999Go; Leyman et al., 2001Go). At least 11 putative TPS genes (encoding trehalose-6-phosphate synthase) are present in the Arabidopsis genome, one of which (TPS1) was shown to encode a functional TPS (Blazquez et al., 1998Go; Leyman et al., 2001Go). In yeast, this reserve carbohydrate and stress protectant has been implicated in the control of glycolytic flux and sugar signaling (Thevelein and Hohmann, 1995Go). Trehalose-6-phosphate is a potent inhibitor of yeast HXK, and there is evidence for the possible involvement of the yeast Tps1 protein itself in controlling glycolytic flux (Bonini et al., 2000Go; Van Vaeck et al., 2001Go). Proper control of Glc influx into glycolysis apparently is required for a wide range of Glc signaling effects in yeast (Van Aelst et al., 1993Go).

In Arabidopsis, inhibition of trehalase causes the accumulation of trehalose and a strong reduction in starch and Suc contents, suggesting a role for trehalose and trehalase in carbon allocation (Müller et al., 2001Go). In addition, trehalose has been shown to inhibit Arabidopsis seedling root elongation and cause starch accumulation in shoots. Furthermore, trehalose increases AGPase (ADP-Glc pyrophosphorylase) activity and induces APL3 gene expression (Wingler et al., 2000Go; Fritzius et al., 2001Go). In soybean, trehalose also affects Suc synthase and invertase activities (Müller et al., 1998Go). How trehalose affects plant gene expression, enzyme activities, photosynthetic activity, and carbon allocation is not clear, but trehalose-6-phosphate does not appear to have any effect on plant hexose phosphorylation (Wiese et al., 1999Go). However, transgenic tobacco plants expressing Escherichia coli homologs of TPS and trehalose-6-phosphate phosphatase show a positive correlation between trehalose-6-phosphate levels and photosynthetic activity, suggesting a regulatory role for trehalose-6-phosphate in plant carbohydrate metabolism (Paul et al., 2001Go).


In contrast to the situation in microorganisms, most downstream components in plant sugar signaling cascades are not well characterized. Some clues to which molecules might be involved come from biochemical and pharmacological studies as well as from obvious analogies to the yeast system.

Protein Kinases and Phosphatases
One of the most common mechanisms in signal transduction is protein phosphorylation and dephosphorylation, and the use of specific inhibitors has indicated the involvement of a variety of PKs and PPs in plant sugar signaling. Extensive pharmacological experiments have been performed in the maize protoplast system to investigate the underlying sugar signaling mechanisms (Sheen, 1993Go, 1999Go; J.-C. Jang and J. Sheen, unpublished data). Inhibitors of PP1 and PP2A mimic the sugar repression of photosynthesis gene promoters (Sheen, 1993Go). This result is consistent with the role of the yeast PP1 (Glc7) in Glc repression (Ludin et al., 1998Go; Alms et al., 1999Go). However, broad-spectrum PK inhibitors and calcium also can block photosynthetic gene expression, suggesting a complex interaction of PKs and PPs (Jang and Sheen, 1997Go). PP inhibitors display a similar effect on photosynthetic genes in photoautotrophic cultures of Chenopodium rubrum (Ehness et al., 1997Go). In the latter system, PP inhibitors as well as Glc- and stress-related stimuli also trigger the activation of stress-inducible invertase and Phe ammonia-lyase gene expression and the rapid and transient activation of putative mitogen-activated protein kinases (Ehness et al., 1997Go). Differential effects of the PK inhibitor staurosporine, however, suggest the involvement of different PKs in sugar and stress signaling pathways. In sweet potato, on the other hand, PP inhibitors block the Suc induction of genes encoding sporamin and {beta}-amylase (Takeda et al., 1994Go), indicating the involvement of different phosphorylation mechanisms in Glc activation. Using a similar pharmacological approach, genes induced by dark and by sugar starvation are controlled differentially by distinct PPs (Fujiki et al., 2000Go). However, these results can be explained by the differential potency of the PP inhibitors used (Sheen, 1993Go).

SNF1, AMP-Activated Protein Kinase, and SnRK in Yeast, Mammals, and Plants
The yeast Snf1 Ser/Thr PK is well characterized as one of the major components in yeast sugar signaling and is required for derepression of a large number of Glc-repressed genes upon sugar starvation (Carlson, 1999Go). Snf1 phosphorylates the transcriptional repressor Mig1, causing its translocation to the cytoplasm and derepression of target genes (De Vit et al., 1997Go; Treitel et al., 1998Go). In addition, Snf1 directly affects the transcription machinery through interactions with the Srb/mediator complex of RNA polymerase II (Kuchin et al., 2000Go) and histone phosphorylation (Lo et al., 2001Go). Snf1 itself is activated by phosphorylation and Glc7 PP1 dephosphorylates and inactivates Snf1 by inducing an autoinhibitory conformational change in the Snf1 complex (Jiang and Carlson, 1996Go). Although yeast Snf1 is not activated by AMP, it is a conserved member and prototype of a family of AMP-activated protein kinases (AMPKs). In mammals, these kinases are involved in protection against environmental and nutritional stresses through signaling of altered cellular AMP/ATP ratios (Hardie and Carling, 1997Go; Hardie et al., 1998Go; Kemp et al., 1999Go). Through derepression of genes involved in the metabolic conversion of alternative carbon sources, Snf1 similarly ensures sufficient ATP synthesis in yeast in the absence of Glc. In addition, Snf1 activation presumably also mediates yeast aging by triggering a shift toward gluconeogenesis and energy storage (Lin et al., 2001Go).

In recent years, biochemical and molecular analysis has revealed the existence of a large family of SnRKs in plants, classified in subgroups SnRK1, -2, and -3 on the basis of amino acid and sequence similarities (Halford and Hardie, 1998Go). Several SnRKs (all SnRK1 class) have been shown to complement the yeast snf1Δ phenotype (Alderson et al., 1991Go; Muranaka et al., 1994Go; Bhalerao et al., 1999Go). Although functional characterization of these proteins is still in an early stage, it is proposed that they act as global regulators of carbon metabolism in plants (Halford and Hardie, 1998Go). Existing data support complex and distinct functions of SnRKs in plants. For example, expression of an antisense SnRK in potato prevents transcriptional activation of a Suc-inducible Suc synthase gene, suggesting its involvement in sugar activation but not repression (Purcell et al., 1998Go). The Arabidopsis pleiotropic regulatory locus (prl1) mutant exhibits transcriptional derepression of a variety of sugar-regulated genes but a sugar-hypersensitive growth phenotype (Nemeth et al., 1998Go).

It has been shown that PRL1 is an inhibitor of the Arabidopsis SnRKs (AKIN10 and AKIN11), and in yeast, its interaction with AKIN10 and AKIN11, based on the two-hybrid assay, is regulated negatively by Glc. However, the prl1 mutation does not seem to affect the regulation of SnRK activity by sugars (Bhalerao et al., 1999Go). The complex interactions of SnRK with PRL1, SKP1/ASK1 (ubiquitin ligase), and a subunit of the 26S proteasome (α4/PAD1) reveal another aspect of SnRK function in protein degradation (Farras et al., 2001Go), which may explain the seemingly contradictory phenotypes in the prl1 mutant (Nemeth et al., 1998Go).

In plants, SnRKs also play an important role in carbon metabolism by directly phosphorylating and inactivating the biosynthetic key enzymes 3-hydroxy-3-methyl glutaryl CoA reductase, nitrate reductase (NR), and Suc phosphate synthase, as shown in vitro (Sugden et al., 1999Go). Phosphorylation of a Suc phosphate synthase peptide by Arabidopsis AKIN kinase complexes also is stimulated by Suc (Bhalerao et al., 1999Go). Interestingly, a SNF1-like gene, together with genes encoding enzymes in primary sugar metabolism (AGPase and Suc synthase), was shown to be expressed asymmetrically in tomato apical meristems, with higher expression levels in the parts destined to form leaves (Pien et al., 2001Go). Like yeast Snf1, plant SnRKs do not seem to be activated directly by AMP. The evidence that some plant SnRKs are activated by sugars and involved in sugar-activated gene expression implies an opposite regulation from that of mammalian AMPKs and yeast Snf1. However, Glc-6-phosphate might act as a negative regulator of SnRK activity (Toroser et al., 2000Go), and AMP appears to inhibit dephosphorylation and the concomitant inactivation of spinach SnRK activity at physiological concentrations (Sugden et al., 1999Go). Therefore, the exact nature of SnRK activation in response to sugars remains unclear. The result that the tobacco SnRK NPK5 is constitutively active in yeast (Muranaka et al., 1994Go) underscores the differential regulation of SnRK activity in yeast and plants.

In both yeast and mammals, Snf1-related PKs are implicated in a variety of distinct regulatory and developmental processes (Hardie and Carling, 1997Go; Carlson, 1999Go; Ashrafi et al., 2000Go; Cullen and Sprague, 2000Go). In plants, several Arabidopsis, wheat, maize, and rice SnRKs from different subfamilies are regulated differentially by light, temperature, cytokinin, developmental stage, and sugars (Takano et al., 1998Go; Ikeda et al., 1999Go; Ohba et al., 2000Go; Chikano et al., 2001Go). Interestingly, the ABA-induced barley SnRK PKABA1 mediates the ABA suppression of GA-induced α-amylase gene expression in aleurone cells (Gomez-Cardenas et al., 2001Go). Expression of antisense SnRK1 in barley anthers causes abnormal pollen development and male sterility (Zhang et al., 2001Go). Finally, a Chlamydomonas SnRK (Sac3) was shown to regulate responses to sulfur limitation (Davies et al., 1999Go).

Further functional analysis of SnRKs can be complicated by redundant functions and multiple interactions with regulatory proteins (Bouly et al., 1999Go; Kleinow et al., 2000Go; Ferrando et al., 2001Go). Yeast Snf1 and mammalian AMPK function in heterotrimeric complexes, consisting of a catalytic protein kinase α-subunit and regulatory {beta}– and γ-subunits. While the regulatory γ-subunit activates the PK by inhibiting the autoinhibitory conformation, the {beta}-subunit acts as an adaptor protein and confers substrate specificity to the complex (Jiang and Carlson, 1996Go, 1997Go; Vincent and Carlson, 1999Go). Although similar complex compositions exist in plants, a novel class of plant SnRKs was identified recently that contains only two components: a Snf1-related kinase subunit and a unique regulatory {beta}γ-subunit, which appears to have developed by domain fusion during plant evolution (Lumbreras et al., 2001Go).

Interestingly, expression of an Arabidopsis cDNA library in yeast has identified several heterologous multicopy suppressors of the snf4 γ-subunit mutant with remarkable functional or structural similarity to yeast suppressor genes (Kleinow et al., 2000Go).

14-3-3 Proteins
The evolutionarily conserved 14-3-3 proteins bind specifically to phosphorylated substrates, thereby controlling enzyme activities, subcellular location, and protein–protein interactions required for signal transduction (Finnie et al., 1999Go; Sehnke et al., 2002Go). A diverse family of 14-3-3 proteins in Arabidopsis interacts with cytosolic enzymes involved in primary nitrogen and carbon metabolic pathways (Bachmann et al., 1996aGo, 1996bGo; Moorhead et al., 1996Go, 1999Go; Toroser et al., 1998Go), with plasma membrane H+-ATPase (Jahn et al., 1997Go), and with the transcriptional machinery (Lu et al., 1992Go). Inactivation of NR by spinach SnRK phosphorylation, for example, requires the presence of a 14-3-3 protein (Bachmann et al., 1996aGo, 1996bGo; Moorhead et al., 1996Go), and in wheat, the WPK4 SnRK both phosphorylates and transfers a 14-3-3 protein to NR (Ikeda et al., 2000Go).

Recently, it was found that 14-3-3 proteins globally regulate the cleavage of their binding partners in sugar-starved Arabidopsis cells. It is proposed that the loss of 14-3-3 protection and the resulting proteolysis underlie the major metabolic shift to reduced nitrate assimilation and sugar synthesis upon sugar starvation (Cotelle et al., 2000Go). Overexpression of 14-3-3 proteins also is associated with enhanced cell survival and delayed senescence, whereas antisense expression results in opposite phenotypes (Markiewicz et al., 1996Go; Wilczynski et al., 1998Go). However, 14-3-3 proteins also were reported to accelerate the degradation of phosphorylated NR (Weiner and Kaiser, 1999Go; Kaiser and Huber, 2001Go), suggesting that the underlying mechanisms might be more complex. Plant trehalose-6-phosphate synthase also interacts with 14-3-3 proteins (Moorhead et al., 1999Go), supporting a role for trehalose-6-phosphate in the starvation response. Loss of 14-3-3 binding might release trehalose-6-phosphate from the trehalose synthesis complex under conditions of low carbon supply (Paul et al., 2001Go).

Like that of NR, the binding of 14-3-3 to Suc phosphate synthase also is regulated by SnRK (Bhalerao et al., 1999Go; Sugden et al., 1999Go). The collaboration of SnRKs and 14-3-3 proteins, therefore, might be more general.

Ca2+ as a Second Messenger
A role for Ca2+ in sugar signaling is suggested by the isolation of a sugar-induced, plasma membrane–associated, calcium-dependent protein kinase in tobacco leaf tissues (Iwata et al., 1998Go). Pharmacological studies with Ca2+ channel blockers (LaCl3), EGTA, and calmodulin inhibitors provide additional evidence for the involvement of Ca2+ signaling in sugar induction of sporamin and {beta}-amylase gene expression in sweet potato (Ohto and Nakamura, 1995Go) and of anthocyanin biosynthesis in Vitis vinifera cell suspension cultures (Vitrac et al., 2000Go). Suc-induced increases in cytosolic levels of free Ca2+ have been shown in transgenic tobacco leaf discs expressing apoaequorin (Ohto and Nakamura, 1995Go). In aequorin-transformed Arabidopsis plants, the moving rate of 14C-Suc (fed to the roots) was reported to be approximately comparable to that of the observed luminescence (Furuichi et al., 2001Go). In the latter study, it was suggested that increases in free cytosolic Ca2+ concentrations could be attributable to membrane depolarization caused by sugar-proton symport. To further elucidate the precise role of Ca2+ in sugar signaling, the development of cellular and genetic tools is necessary (Sheen, 1996Go; Allen and Schroeder, 2001Go).


Although the biochemical approach has revealed the involvement of PPs and PKs, including PP1, SnRK, calcium-dependent protein kinase, mitogen-activated protein kinase, and the second messenger Ca2+, in plant sugar signaling, the targets of these regulatory molecules and their physiological functions remain elusive. A genetic approach using Arabidopsis as a model plant offers distinct strategies to dissect the complex mechanisms that underlie sugar sensing and signaling in plants. Based on either sugar-regulated gene expression or sugar-insensitive or sugar-oversensitive phenotypes during germination and seedling development (Figure 4) , a large collection of sugar signaling mutants has been isolated in Arabidopsis (summarized in Tables 1 and 2) (Sheen et al., 1999Go; Gibson, 2000Go; Smeekens, 2000Go; Rook et al., 2001Go).

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Figure 4. Arabidopsis Seedling Phenotypes on High-Glc Medium.Wild-type (WT), Glc-insensitive (gin), and Glc-oversensitive (glo) plants were grown on 6% Glc Murashige and Skoog (1962)Go medium for 5 days under light.

Although the designs for genetic screens are different, many independently isolated sugar-insensitive mutants are allelic, suggesting the use of conserved mechanisms in plant sugar responses. For example, the Glc-insensitive gin1 mutant is allelic to sis4 (sugar insensitive) and isi4 (impaired sugar induction), gin4 is allelic to sis1, and gin6 is allelic to sun6 (Suc uncoupled), sis5, and isi3 (Table 2) (Sheen et al., 1999Go; Gibson, 2000Go; Smeekens, 2000Go; Rook et al., 2001Go). With the exception of the prl1 mutant, most mutants that show hypersensitivity to Glc (glo and gss) or Suc (sss) have not been well characterized. Further phenotypic analyses of these sugar-hypersensitive mutants and the unique sugar-insensitive mutants, and molecular cloning of their corresponding genes, will reveal new mechanisms of sugar regulation.

The most surprising and exciting outcome of the genetic, phenotypic, and molecular characterization of Glc-insensitive mutants is the extensive and direct interactions between sugar and hormonal signaling (Figure 5) . The observation that the “gin” phenotype can be mimicked by 1-aminocyclopropane-1-carboxylic acid (the immediate ethylene precursor) treatment of wild-type seedlings on 6% Glc Murashige and Skoog (1962)Go plates prompted the investigation of interactions between sugar and ethylene signaling (Zhou et al., 1998Go). The constitutive ethylene biosynthesis (eto1) and constitutive ethylene signaling (ctr1) mutants are insensitive to Glc repression of cotyledon and shoot development, similar to gin1. These findings have been further confirmed by the isolation of new alleles of ctr1, including gin4 and sis1 (Table 2) (Gibson et al., 2001Go; W.-H. Cheng and J. Sheen, unpublished data). However, unlike eto1 and ctr1, gin1 does not display the triple response phenotype in the dark, a typical ethylene response (Roman et al., 1995Go), suggesting that the gin phenotype and the triple response can be uncoupled (Figure 5).

Genetic Model of Interactions between Sugar and Hormone Signaling in Arabidopsis.The gin phenotype (shown in Figure 4) is mimicked by ethylene precursor treatment of wild-type plants and is displayed in constitutive ethylene biosynthesis (eto1) and constitutive ethylene signaling (ctr1) mutants, whereas the ethylene-insensitive mutants etr1-1 and ein2 exhibit the glo phenotype (shown in Figure 4). Epistasis analysis with the gin1 etr1 and gin1 ein2 double mutants puts GIN1 downstream of the ETR1 receptor and EIN2 (Zhou et al., 1998Go; W.-H. Cheng and J. Sheen, unpublished data). Thus, Glc and ethylene signaling pathways antagonize each other (Zhou et al., 1998Go; W.-H. Cheng and J. Sheen, unpublished data). However, the triple response is not affected by Glc. The gin1, sis4, and isi4 mutants are allelic to aba2 (Laby et al., 2000Go; Rook et al., 2001Go; W.-H. Cheng and J. Sheen, unpublished data). ABA2 encodes a short-chain dehydrogenase/reductase (SDR1) that is involved in the second to last step of ABA biosynthesis (Rook et al., 2001Go; W.-H. Cheng and J. Sheen, unpublished data; P.L. Rodríguez, personal communication; Seo and Koshiba, 2002Go) and is controlled directly by Glc (W.-H. Cheng and J. Sheen, unpublished data). Other ABA-deficient mutants (aba1-1, aba2-1, and aba3-2) also are Glc insensitive (Arenas-Huertero et al., 2000Go; Huijser et al., 2000Go; Laby et al., 2000Go). ABA1 and ABA3 are important for ABA biosynthesis and are regulated directly by Glc (W.-H. Cheng and J. Sheen, unpublished data). Characterization of the gin5 mutant shows the requirement of Glc-specific ABA accumulation for HXK-mediated Glc signaling (Arenas-Huertero et al., 2000Go). In addition, gin6, sun6, sis5, and isi3 are allelic to abi4, an ABA-insensitive mutant (Arenas-Huertero et al., 2000Go; Huijser et al., 2000Go; Laby et al., 2000Go; Rook et al., 2001Go). Glc activation of ABI4, which encodes an AP2 domain transcription factor (Finkelstein et al., 1998Go), requires ABA, although ABI4 is not induced by ABA directly (Arenas-Huertero et al., 2000Go; Soderman et al., 2000Go; W.-H. Cheng and J. Sheen, unpublished data). The abi5 mutant also is Glc insensitive. Glc activates ABI5 directly (W.-H. Cheng and J. Sheen, unpublished data), encoding a basic Leu zipper transcription factor (Finkelstein and Lynch, 2000bGo). However, other ABA-insensitive signaling mutants (abi1-1, abi2-1, and abi3-1) do not exhibit the gin phenotype, as do abi4 and abi5 mutants (Arenas-Huertero et al., 2000Go; Huijser et al., 2000Go; Laby et al., 2000Go), suggesting that a distinct ABA signaling pathway is involved in Glc signaling. In summary, Glc activates ABA biosynthesis and ABA signaling, and both antagonize ethylene signaling (W.-H. Cheng and J. Sheen, unpublished data). It remains possible that Glc also inhibits ethylene signaling directly. The AtHXK1 mutant (gin2) affects ABA and ethylene signaling but also displays reduced sensitivity to auxin and increased sensitivity to cytokinin (L. Zhou and J. Sheen, unpublished data).

Interestingly, overexpression of the C terminus of EIN2 (ethylene insensitive) shows many constitutive ethylene phenotypes but not the triple response (Alonso et al., 1999Go). Many (but not all) ethylene-insensitive mutants, including etr1, ein2, ein3, and ein6, also exhibit Glc hypersensitivity (Zhou et al., 1998Go; W.-H. Cheng and J. Sheen, unpublished data). Double mutant analyses suggest that GIN1 acts downstream of the ethylene receptor ETR1 and HXK (Figure 5) (Zhou et al., 1998Go; W.-H. Cheng and J. Sheen, unpublished data). Future research should focus on understanding the precise molecular link between Glc and ethylene signaling through the analysis of more double mutants and the biochemical characterization of known signaling components (Sheen et al., 1999Go; Bleecker and Kende, 2000Go; Stepanova and Ecker, 2000Go).

The HXK-mediated Glc signaling pathway is connected not only to the ethylene pathway but also to the ABA pathway. The gin1 mutant is known to be allelic to aba2 (Laby et al., 2000Go; Rook et al., 2001Go; W.-H. Cheng and J. Sheen, unpublished data; P.L. Rodríguez, personal communication), a classic Arabidopsis mutant with deficiency in ABA biosynthesis (Schwartz et al., 1997Go; Koornneef et al., 1998Go). The ABA2 gene was found recently to encode a short-chain dehydrogenase/reductase (SDR1) that catalyzes the second to last step of the major endogenous ABA biosynthesis pathway (W.-H. Cheng and J. Sheen, unpublished data). This surprising result indicates that Glc can modulate ethylene signaling through the ABA pathway. This finding also is consistent with the recent discovery that the gin6 mutant is allelic to abi4 (Arenas-Huertero et al., 2000Go), an AP2 domain transcription factor (Finkelstein et al., 1998Go). Independent genetic, phenotypic, and molecular analyses of the sun6 (Huijser et al., 2000Go), sis5 (Laby et al., 2000Go), and isi3 (Rook et al., 2001Go) sugar signaling mutants have revealed their allelism to gin6/abi4. Similar studies also have confirmed that gin1/aba2 is allelic to the sugar signaling mutants sis4 (Laby et al., 2000Go) and isi4 (Rook et al., 2001Go) (Table 2). In addition, overexpression of the Arabidopsis ABA-responsive element (ABRE) binding factors ABF3 or ABF4 confers both ABA and glucose oversensitive phenotypes, supporting an intimate interaction between glucose and ABA signaling (Kang et al., 2002Go).

It is now clear that HXK-mediated Glc signaling is connected to ethylene and ABA signaling. Further analyses show that Glc modulates genes involved in ABA biosynthesis and signaling (Figure 5) (Arenas-Huertero et al., 2000Go; W.-H. Cheng and J. Sheen, unpublished data) as well as ethylene signaling (W.-H. Cheng and J. Sheen, unpublished data). Moreover, a sugar-induced increase in ABA synthesis may be required for HXK-dependent sugar signaling (Figure 5) (Arenas-Huertero et al., 2000Go). A connection between ABA and ethylene signaling is supported further by the recent isolation of alleles of ctr1 and ein2 as enhancer and suppressor mutations of abi1, respectively (Ghassemian et al., 2000Go). In addition, the era3 mutant (enhanced response to ABA) is allelic to ein2 (Beaudoin et al., 2000Go). These studies dramatically illustrate the fact that ABA and ethylene signaling pathways antagonize each other during germination and seedling development. At lower sugar concentrations, the ABA inhibition of germination is reduced by sugars (Finkelstein and Lynch, 2000aGo). Thus, hormone and sugar signaling networks may have different links depending on cell types, developmental stages, physiological state, and environmental cues.

The isolation of the Arabidopsis gin2 mutant provides genetic evidence for a direct link between AtHXK1 and sugar sensing and signaling, suggested previously by biochemical, molecular, and transgenic analyses (Jang and Sheen, 1994Go, 1997Go; Pego et al., 1999Go) (Figure 3). Phenotypic analyses of the gin2 mutant, in addition, reveal a new connection between sugar and auxin/cytokinin signaling that is independent from ethylene and ABA signaling (Figure 5). Further characterization of the auxin and cytokinin signaling components (Guilfoyle et al., 1998Go; Gray and Estelle, 2000Go; Hwang and Sheen, 2001Go; Mok and Mok, 2001Go) should reveal the molecular mechanisms that underlie their interactions with the sugar signal transduction pathway. The characterization of enhancer and suppressor mutations of gin2 also will be a useful approach to further elucidate HXK action.


Consistent with the pleiotropic effects of sugars on plant metabolism, growth and development, stress response, and gene expression, a complex picture of sugar-controlled regulatory networks and interactions with multiple signaling pathways is emerging. Although biochemical studies provide evidence for the involvement of a variety of protein kinases, protein phosphatases, 14-3-3 proteins, and Ca2+ as a second messenger, and although several transcription factors and regulatory cis elements have been found to mediate sugar control of gene expression, their precise roles in sugar signal transduction pathways require further investigation. Significant progress has been made with the identification of AtHXK1 as a sugar sensor, the possible involvement of SnRKs in sugar and metabolite signaling, and the identification of sugar signaling mutants as components in plant hormone biosynthesis and signal transduction.

Elucidation of the complete signaling circuitry that underlies the complex biological responses to changing sugar levels is challenging for a number of reasons. First, there is the intrinsic complexity of a multicellular photosynthetic organism with both source and sink tissues and with sugar producing and consuming activities. As a consequence, research is focused on multiple model systems and different cell types, further complicating direct comparison of experimental results. Different species also display distinct source-sink relationships and nutrient uptake, transport, and utilization mechanisms. For example, potato plants have a strong tuber sink and generally show less prominent sugar-related symptoms in source leaves. Sugar-related symptoms usually are also less pronounced in Arabidopsis leaves than in tobacco or tomato leaves, perhaps as a result of differences in plant architecture and leaf nitrogen allocation (von Schaewen et al., 1990Go; Dai et al., 1999Go). In addition, plants can display different sensitivities to endogenous and external signals at different developmental stages. Therefore, mesophyll cells of young and old leaves respond to sugars differently (Sheen, 2001Go).

Finally, genetic analysis in plants has been far more difficult than in the simple unicellular yeast system. However, the establishment of Arabidopsis as a plant model with the availability of the complete genome sequence, knockout lines, and microarray technology has boosted genetic research in plant signal transduction (Arabidopsis Genome Initiative, 2000Go; Bleecker and Kende, 2000Go; McCarty and Chory, 2000Go; Richmond and Somerville, 2000Go; Sussman et al., 2000Go; Zhu and Wang, 2000Go; Schroeder et al., 2001Go). The comparison of global gene expression profiles between sugar mutant and wild-type plants will reveal novel signaling mechanisms and facilitate the dissection of downstream interacting pathways mediating ABA, auxin, cytokinin, ethylene, and nitrogen regulation. The design of more specific genetic screens, such as the isolation of suppressor and enhancer mutations of the gin2 mutant, may lead to new mechanisms of HXK action in the protein complexes and in interacting proteins. Genetic evidence for the functions of PKs, PPs, Ca2+, G proteins, and sugar sensors other than HXK will be required to fill in the gaps in the sugar signaling network. Further development of physiological cell systems will power the analyses of molecular and biochemical mechanisms underlying interactions between signaling pathways. Because of its central role in plant signal transduction, insight into sugar sensing and signaling and the control of carbon allocation offer the possibility of important biotechnological applications.

source:Li Zhou

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Thanks to alert reader Glen for pointing out that the FDA already has a regulation for Corn Sugar in the Code of Federal Regulations, under food substances Generally Recognized as Safe (GRAS). CFR Section 184.1857 reads:


(a) corn sugar (C6H12O6, CAS Reg. No. 50-99-7), commonly called D-glucose or dextrose, is the chemical [alpha]-D-glucopyranose. It occurs as the anhydrous or the monohydrate form and is produced by the complete hydrolysis of corn starch with safe and suitable acids or enzymes, followed by refinement and crystallization from the resulting hydrolysate.

(b) The ingredient meets the specifications of the Food Chemicals Codex, 3d Ed. (1981), pp. 97-98 under the heading “Dextrose….”

(c) In accordance with 184.1(b)(1), the ingredient is used in food with no limitation other than current good manufacturing practice.

The Corn Refiners have just petitioned the FDA to be allowed to use the name Corn Sugar to apply to both glucose/dextrose and High Fructose Corn Syrup (HFCS). But the existing definition seems to exclude HFCS. While HFCS is about half glucose, it is also about half fructose, and its manufacture from corn starch requires one more enzyme.

A reminder about sugar chemistry:

sucrose table sugar

The Four Sugars

Glucose is the sugar in blood, and dextrose is the name given to glucose produced from corn. Biochemically they are identical.

Fructose is the principal sugar in fruit. In fruit, it raises no issues because it is accompanied by nutrients and fiber.

Sucrose is table sugar. It is a double sugar, containing one part each of glucose (50%) and fructose (50%), chemically bound together. Enzymes in the intestine quickly and efficiently split sucrose into glucose and fructose, which are absorbed into the body as single sugars.

HFCS is made from corn starch. It contains roughly equivalent amounts of glucose (45 to 58%) and fructose (42 to 55%).

HFCS raises several issues, health and otherwise:

Concerns about High Fructose Corn Syrup

high fructose corn syrup soda with straw

Quantity: the U.S. food supply provides to every American (all ages) about 60 pounds of sucrose and another 60 pounds of HFCS each year. This is way more than is good for health. Sugars of any kind provide calories but no nutrients.

Fructose: increasing evidence suggests that the metabolism of fructose–which differs from that of glucose–is associated with abnormalities. This means that it is best to reduce intake of fructose from table sugar as well as HFCS.

Farm subsidies: these go to large corn producers and have kept down the cost of HFCS relative to that of sucrose. The use of corn to make ethanol has raised the relative price of HFCS.

Genetic modification: Most corn grown in the United States is genetically modified to resist insects or herbicides.

From a health standpoint, it makes no difference whether the sweetener is sucrose or HFCS.

As for agave sugar as a substitute: it can have much higher concentrations of fructose than either sucrose or HFCS but its labels do not give percentages so you have no way to know how much.

Given all this, what’s your guess about what the FDA will decide?

Source:Marion Nestle

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The WHO’s Recommendation: 12 Teaspoons of Free (Added) Sugar Daily

Most teenage males consume an average of 34 teaspoons (136 grams) of sugar per day, mostly from the soft drinks, according to the US Department of Agriculture (USDA).

For example, the 1999 figure for added-sugars consumption was 1.5 percent greater than in 1998.

Consumption of “added sugars” includes:

  • table sugar (refined, processed sugars from cane, beet – sucrose – added to foods by the manufacturer, cook or consumer)
  • corn sugar (glucose)
  • corn syrup
  • high-fructose corn syrup commonly added to fruit juices
  • sugars naturally present in fruint juices
  • honey, and
  • other syrups, like molasses and maple syrup.

The term “added sugars” does not include the sugars naturally present in:

  • milk (lactose)
  • fruit (fructose, sucrose), and
  • vegetables.

A report released in 2006 by the World Health Organization (WHO) urges people to limit their daily consumption of free (added) sugars to less than 10 percent of their total energy intake (Diet Nutrition and the Prevention of Chronic Diseases; TRS916). This recommendation adds up to approximately 12 teaspoons (48 grams) of added (free) sugar a day based on an average 2000-calorie diet.

In North America, however, this report prompted a harsh reaction from the sugar lobby.

The leading American health experts want the FDA to set a maximum recommended daily intake (Daily Value) for added (free) sugars of 10 teaspoons (40 grams) and require labels to disclose the percentage of the Daily Value a food provides. (Daily Values are used on Nutrition Facts labels to indicate the recommended maximum intakes of fat, sodium and other nutrients).

It is so much less than North Americans eat now – on average, more than 20 teaspoons of added sugars per day, that is twice what the U.S. Department of Agriculture recommends.

Although we are eating way too much sugar, consuming less sugar is not that easy as it would seem. Cutting back to 10 – 12 teaspoons a day is going to be tough.

A typical cup of fruit yogurt provides 70 percent of a day’s worth of added sugar! No to mention a can of baked beans, listing white beans, water, molasses, sugar, fructose, brown sugar. Lots of sugars!

Of course, you would like to have these beans with a hot dog which lists such ingredients as pork, chicken, beef, water, salt, dextrose. It means more sugar!

The bun contains another half-teaspoon of sugar. And with that hot dog you would like to have a dash of ketchup (a third of ketchup is sugar)…

Another example: a health snack – granola bar has two teaspoons of sugar.

One little Fruit Rollup, Mellon Berry Blast has about 3 teaspoons of sugar, mostly in form of cheap corn syrup.

The WHO report recommending we eat less sugar provoked loud criticism from the sugar lobby in the U.S. and Canada.

The sugar industry and the American government are really upset about it. Randall Kaplan of the Canadian Sugar Institute says that there is no scientific proof sugar is what is making us fat or giving us diabetes (!)

According to USDA data, people who eat diets high in sugar get less calcium, fiber, folate, vitamin A, vitamin C, vitamin E, zinc, magnesium, iron, and other nutrients.

Although presently it cannot be proved “scientifically” that sugar along is to blame, there’s plenty of evidence that it is the key contributing factor.Onset of diabetes, for instance, is one of the major concerns for excess sugar intake. Since insulin acts as a “carrier” of glucose (blood sugar), too much sugar can overwork the pancreas, eventually leading to a decrease in insulin production.

Because of such potential problems, the Center for Science in the Public Interest (CSPI) has petitioned the FDA to require that food labels declare how much sugar is added to products.

A high-sugar diet can contribute to other health problems, such as osteoporosis, cancer, and heart disease, not to mention tooth decay and obesity.

Unfortuanately, nutritionally worthless junk food is everywhere. No matter what, in every store that you go to there is a little section of chocolate, candy and chips. Sugar is all over the place and it is hard to resist it.

Simple (Free) Sugars Consumption and Sugar Cravings
An intense desire to consume simple sugars is commonly known as carbohydrate or sugar (sucrose) cravings. Ironically, it is believed to occur as a result of rapid rises and subsequent rapid falls in blood sugar which are caused by… high consumption of simple sugars (carbohydrates).In the typical diet of the USA population, the major contributing factors in sugar cravings include:

  • Soft drinks – their consumption is responsible for 33 percent of the total content of added (free) simple sugars
  • Sweetened grains (primarily breakfast cereals) – their consumption is responsible for 19 percent of the total content of added (free) simple sugars
  • Sweets/candy – their consumption is responsible for 17 percent of the total content of added (free) simple sugars
  • Fruit drinks – their consumption is responsible for 10 percent of the total content of added (free) simple sugars
  • Milk products – their consumption is responsible for 9 percent of the total content of added (free) simple sugars

Unfortunately, many people are actually addicted to sugar. In order to free yourself of the physical addiction, complete avoidance of all sugar is necessary. Complete abstinence resolves the biochemical addiction, however, during this transition it is very important to eat every two-three hours to avoid symptoms of hypoglycemia.

If you do not eat every 2-3 hours your blood sugar may “crash” and you’ll feel horrible. Usually, this is necessary for several days to several weeks.

However, carbohydrate (sugar) cravings may be also caused by metabolic and nervous system ailments such as:

  • Hypoglycemia, a “catch-22” disease where insulin over-counteracts high blood sugar/blood glucose levels, leading to low blood sugar/blood glucose, leading to a craving for… more sugar;
  • Obesity – excessive body fat, a term applied to persons who are more than 20 percent above their recommended body weight as measured by body mass index (BMI);
  • Bulimia, a type of eating disorder where the afflicted person eats large amounts of food, then self-induces vomiting;
  • Depression – sadness and unhappiness;
  • Seasonal Affective Disorder (SAD), a type of depression that usually occurs during autumn or winter as a result of insufficient exposure to the ultra-violet radiation present in sunlight;
  • Stress, due to worry, injury or disease.

The other possible causes of sugar (carbohydrate) cravings also include:

  • Pre-Menstrual Syndrome (PMS), a combination of ailments that can appear at any time during the two weeks (most commonly during the last four days) preceding menstruation;
  • Excessive proliferation of Candida albicans, one of 70 different species of Candida yeast present in the mouth, esophagus, intestines or vagina.

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How to Decipher Sugar Content?
Nutrition label to disclosing the percentage of the Daily Value a sugar.

Current food labels do not spell out exactly how much of the most common nutrients we’re getting. Carbohydrates do not include totals for fibers and sugars. So we just have to rely on the list of ingredients to determine how many sugars are in the foods we eat.

In order to estimate the total number of sugars found in foods, experts use a teaspoon of refined sugar as a metaphor to give us a sense of how much sugar we’re consuming. Therefore, a product which contains 16 grams of sugars per serving would translate into approximately 4 teaspoons of sugars per serving.

In every teaspoon/serving size, there are 4 grams of refined sugar, providing on average 15 calories.

In other words, in order to determine how much sugar is in a serving, you need to check the nutrition label for Sugars (listed in grams) and divide the number of grams by four. For example, if sugars are listed as 12 grams you should divide that amount by four and this will give you three teaspoons of refined sugar per serving – and 45 calories.

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How to Reduce Your Sugar Intake?

If we were eating just all vegetables and some low-sweet fruits, and getting our sugars just from there, we would be way better off.

First of all, check nutrition and ingredient labels for sugar and its equivalents, including sucrose, high-fructose corn syrup, corn syrup, dextrose, glucose, fructose, maltose, honey and molasses.

At present, the USDA recommends limiting added sugars, from packaged foods and the sugar bowl, to:

  • 24 grams a day (6 teaspoons) if you eat 1,600 calories
  • 40 grams (10 teaspoons) for a 2,000-calorie diet
  • 56 grams (14 teaspoons) for a 2,400-calorie diet, and
  • 72 grams (18 teaspoons) for a 2,800-calorie diet.

As you can see, this is even less than 12 teaspoons (48 grams) of a sugar a day recommended by the recent WHO’s report for an average 2,000-calorie diet.

What you should do then? First of all, cut back on:

  • soft drinks (40 grams of sugar per 12 ounces) – nutritionally empty “liquid candy” – by far the biggest source of sugar in the average American’s diet
  • fruit “drinks,” “beverages,” “ades,” and “cocktails” as they are essentially non-carbonated soda pop; Sunny Delight, Fruitopia, and other fruit juices have only 5-10 percent juice and are loaded with calories and can be as fattening as pop
  • candy, cookies, cakes, pies, doughnuts, granola bars, pastries, and other sweet baked goods
  • fat-free cakes, cookies, and ice cream as they may have as much added sugar as their fatty counterparts and they’re often high in calories (“fat-free” on the package doesn’t mean fat-free on your waist or thighs).

Instead drink purified, filtered water, eat more vegetables and have few low-sweet fruits.

Look for breakfast cereals that have no more than eight grams (about 2 teaspoons) of sugar per serving.

Watch out for sweets – ice cream, shakes, and pastries – served in restaurants. Their huge servings can provide a day’s worth of added sugar. For example, a large McDonald’s Vanilla Shake and a Cinnabon each have 12 teaspoons (about 48 grams) of added (free) sugar.

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Getting That Sugar Monkey Off Your Back: More Tips
  • Don’t avoid sugar like the plague. Demystify it. Sugar is neither evil nor your friend. Nutritionally speaking, when you eat sugar, you get only empty calories. There are no virtues associated with sugar.
  • Eat regular meals. Having small meals every two-three hours will keep your blood glucose levels stable.
  • Don’t overeat. Just eat appropriate foods at appropriate times. You are less likely to go overboard when you have a full meal in your stomach.
  • Wait five minutes and see if the craving passes. If it doesn’t, have a single serving of what you want, instead of a “healthy substitute.” Substitutions do not always work. If you really want ice cream, you’re better off having a little ice cream than three pounds of carrot sticks.
  • Don’t use sweet treats as a distraction. When you find yourself reaching for the jelly beans, ask yourself what’s going on. If you’re hungry, have the kind of snack that will last longer than a sugar rush — some almonds, for instance. If you’re stressed, take a walk. If you’re sad, call a friend. If you’re bored, get out of the house.
  • Don’t full yourself into thinking you can eat more of other foods because you have downed a diet soft drink or put artificial sweetener in your coffee.
  • Get rid of the candy dish on your desk and the stash of Ring-Dings in your kitchen. If junk food isn’t around, you can’t eat it. When you want a sugary snack, go out and buy – one only.
  • Get more pleasure out of a piece of higher quality chocolate rather than out of a bag of Hershey’s kisses every other day. If you can get into the habit of having a little of your favorite sweet thing every day, you may be less likely to “lose control” and work your way through the candy counter.

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What About Fruit Sugar (Fructose)?

Fructose is incorporated into triglycerides more readily than glucose (blood sugar); therefore, it has a greater propensity to increase serum triglycerides.

Fructose, also known as fruit sugar (levulose) is a simple sugar twice as sweet as sucrose (table sugar). But because it is mainly metabolized in the liver, fructose has a lower glycemic index.

However, consumption of high amounts of fructose can lower metabolic rate and cause de-novo lipogenesis (the conversion of sugar into fat) since the liver can only metabolize limited amounts of fructose. For this and many other reasons, and contrary to previous claims for its superiority over glucose (blood sugar), fructose does not play essential part in human nutrition.

Although naturally present in fruits, fructose is also available in the form of crystals as a table sugar substitute. It is also sold commercially as high-fructose corn syrup which can contain up to 55 percent sucrose.

However, fructose can have some toxic effects on our health, especially on cardiovascular and digestive systems, as well as on our metabolism.

Fructose, especially its excessive consumption, may increase:

  • the risk of abnormal blood clotting ailments and hypertension (high blood pressure)
  • the risk of type 2 diabetes
  • total blood cholesterol levels (it serves in part as the raw material for the synthesis of cholesterol within the body)
  • LDL-“bad” cholesterol levels, and
  • blood triglyceride levels, especially in diabetics (fructose has a greater propensity to increase serum triglycerides than glucose).

Excessive consumption of fructose may also cause:

  • fatigue, especially in persons who are fructose intolerant
  • insulin resistance, and
  • obesity (due to de-novo lipogenesis – the conversion of sugar into fat).

It is estimated that up to 33 percent of persons are unable to completely absorb fructose due to fructose intolerance (also known as dietary fructose intolerance (DFI) which may cause

  • flatulence (gas)
  • intestinal cramps (abdominal pain)
  • bloating, and
  • altered bowel habits (diarrhea).

Fructose may cause the symptoms of irritable bowel syndrome (IBS) and may be an underlying cause of some cases of IBS due to fructose malabsorption.

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Fruit Sources of Fructose
FRUIT LIST Fructose per 100 grams
1. Dates 32 grams/32%
2. Raisins 29.7 grams/27.9%
3. Figs 22.9 grams/22.9%
4. Prunes 12.5 grams/12.5%
5. Grapes 8.13 grams/8.13%
6. Pears 6.23 grams/6.23%
7. Cherries 6 grams/6%
8. Apples 5.9 grams/5.9%
9. Persimmon 5.56 grams/5.56%
10. Blueberry 4.97 grams/4.97%
11. Bananas 4.85 grams/4.85%
12. Kiwi Fruit 4.350 grams/4.35%
13. Watermelon 3.36 grams/3.36%
14. Plums 3.07 grams/3.07%
16. Honeydew Melon 2.96 grams/2.96%
17. Grapefruit 2.5 grams/2.5%
18. Strawberry 2.5 grams/2.5%
19. Blackberry 2.4 grams/2.4%
20. Raspberry 2.35 grams/2.35%
21. Orange 2.25 grams/2.25%
22. Pineapple 2.05 grams/2.05%
23. Cantaloupe 1.87 grams/1.87%
24. Peach 1.53 grams/1.53%
25. Nectarine 1.37 grams/1.37%
26. Apricot 0.94 gram/0.94%

As you can see, among the twenty-six popular fruits the lowest fructose content show, respectively:

    • apricots
    • nectarines
    • peaches


  • cantaloupes.

Therefore, the above fruits should be your first choice of fruit in triglycerides-lowering diet, provided you have not been diagnosed with fructose intolerance.

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Fruit Sources of Sucrose
FRUIT LIST Sucrose per 100 grams
1. Papaya 30 grams/30%
2. Dates 20 grams/20%
3. Apricot 5.87 grams/5.87%
4. Pineapple 5.47 grams/5.47%
5. Nectarine 4.87 grams/4.87%
6. Peach 4.76 grams/4.76%
7. Cantaloupe 4.35 grams/4.35%
8. Orange 4.28 grams/4.38%
9. Honeydew Melon 2.48 grams/2.48%
10. Bananas 2.39 grams/2.39%
11. Apples 2.07 grams/2.07%
12. Plums 1.57 grams/1.57%
13. Persimmon 1.54 grams/1.54%
14. Watermelon 1.21 grams/1.21%

As you can see, among the fourteen popular fruits the lowest sucrose (sugar) content show, respectively:

  • watermelons
  • persimmons (juicy smooth-skinned orange-red tropical fruits that are sweet only when fully ripe) and
  • plums.

Therefore, the above fruits should be your first choice of fruit in triglycerides-lowering diet, provided you have not been diagnosed with fructose intolerance.

Logical, isn’t it? But not necessarily true.

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Lowering High Triglycerides: Your Choice of Fruit
Whole fruits are both a source of fructose and – sucrose, in other words, sugar. Also known as beet or cane (table) sugar, chemically it consists glucose and – fructose.Glucose is the only carbohydrate that actually circulates within the bloodstream (as blood sugar). It provides energy to most of the body’s cells and is the preferred fuel for most cells, including the neurons of the brain (the brain utilizes 25 percent of glucose for its own “fuel” requirements).

Sugar then is a sort of “good” and “bad” guy at the same time with fruits as a perfect example. Some of them are high in fructose but at the same time low in sucrose, and vice versa.

Watermelon, for instance, is low in sucrose (1.21%) but at the same time much higher in fructose (3.36%). Apricots on the other hand are low in fructose (0.94%) but very high in sucrose (5.87%). The same applies to other low-high, fructose-sucrose fruits like persimmons, plums, nectarines, peaches and cantaloupes.

So as far as fruit consumption is concerned, the only practical solution is their limited consumption. Because fruits are a considerable source of sugar in our today’s diet (already full of sugar!), their daily intake should be carefully monitored by all people, not only those whose health condition could be adversely affected by the sugar, diabetics and pre-diabetics in particular.

Like with many other things in our life, moderation is the key here, the only win-win situation. And this “rule” should be followed by everyone who is seriously concerned about his or her health.

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Table of Fruits and Sugars

Tomatoes, avocadoes, lemons and limes are very low in total sugar and do not have to be restricted.

Although eating fresh fruits as your appetite dictates still holds for many people, if you are overweight, insulin resistant, or have elevated blood triglycerides, you should limit your intake of high-sugar fruits, such as grapes, bananas, mangos, sweet cherries, apples, pineapples, pears and kiwi fruit.

This recommendation also applies to dried fruits which contain excessive sugar. As a matter of fact, they more resemble commercial candy than their fresh counterparts.

Try to include more vegetables instead. However, some fruits, like tomatoes, avocadoes, lemons, and limes, are very low in total sugar and do not have to be restricted.

Fructose consumption is particularly problematic for people who are insulin resistant – a condition associated with metabolic syndrome X and/or type 2 diabetes. Because sucrose (table sugar) is split in the gut into its two component parts (fructose and glucose) before it enters the bloodstream, sucrose’s contribution to the total dietary fructose load must be considered.

For this reason the total metabolic fructose for items below has been tabulated (in grams of sugar per 100 grams). The term “total metabolic fructose” (Tot. met. fructose) means fructose and sucrose combined.

TOTAL Sugars Glucose Galactose Fructose Sucrose Lactose Maltose Tot. Met. Fructose
Fresh Fruit
Apples 13.3 2.3 7.6 3.3 9.3
Apricots 9.3 1.6 0.7 5.2 3.1 3.3
Avocado, California 0.9 0.5 0.2 0.1 0.3
Avocado, Florida 0.9 0.5 0.2 0.1 0.3
Banana 15.6 4.2 2.7 6.5 6.0
Blackberries 8.1 3.1 4.1 0.4 4.3
Blueberries 7.3 3.5 3.6 0.2 3.7
Cantaloupe 8.7 1.2 1.8 5.4 4.5
Casaba melon 4.7 0.3 0.0
Cherries, sweet 14.6 8.1 6.2 0.2 1.3 6.3
Cherries, sour 8.1 4.2 3.3 0.5 3.6
Elderberries 7.0
Figs 6.9 3.7 2.8 0.4 3.0
Grapefruit, pink 6.2 1.3 1.2 3.4 2.9
Grapefruit, white 6.2 1.3 1.2 3.4 2.9
Grapes 18.1 6.5 0.4 7.6 0.1 7.6
Guava 6.0 1.2 1.9 1.0 0.7 2.4
Guava, strawberry 6.0 1.2 1.9 1.0 2.4
Honeydew melon 8.2
Jackfruit 8.4 1.4 1.4 5.4 4.1
Kiwi fruit 10.5 5.0 4.3 1.1 4.9
Lemon 2.5 1.0 0.8 0.6 1.1
Lime 0.4 0.2 0.2 0.2
Mamey Apple 6.5 1.1 3.7 1.6 4.5
Mango 14.8 0.7 2.9 9.9 7.9
Nectarine 8.5 1.2 6.2 3.1
Orange 9.2 2.2 2.5 4.2 4.6
Papaya 5.9 1.4 2.7 1.8 0.4 3.6
Peach 8.7 1.2 1.3 5.6 4.1
Pear 10.5 1.9 6.4 1.8 7.3
Pear, Bosc 10.5 1.9 6.4 1.8 7.3
Pear, D’Anjou 10.5 1.9 6.4 1.8 7.3
Pineapple 11.9 2.9 2.1 3.1 3.7
Plum 7.5 2.7 1.8 3 3.3
Pomegranate 10.1 5.0 4.7 0.4 4.9
Purple Passion Fruit or Granadilla 11.2 4.0 3.1 3.3 4.8
Raspberries 9.5 3.5 3.2 2.8 1.0 4.6
Starfruit 7.1 3.1 3.2 0.8 0.1 3.6
Strawberries 5.8 2.2 2.5 1.0 3.0
Tangerine 7.7
Tomato 2.8 1.1 1.4 1.4
Watermelon 9.0 1.6 3.3 3.6 5.1
Dried Fruit
Dates 64.2 44.6 22.3
Dried apricots 38.9 20.3 12.2 6.4 15.4
Dried figs 62.3 26.9 3.9 24.4 6.1 27.5
Dried mango 73.0
Dried papaya 53.5
Dried peaches 44.6 15.8 15.6 13.2 22.2
Dried pears 49.0
Dried prunes 44.0 28.7 14.8 0.5 15.1
Raisins 65.0 31.2 33.8 33.8
Raisins, Golden 70.6 32.7 37.1 0.8 37.5
Zante currants 70.6 32.7 37.1 0.8 37.5
Pure sugars
Sucrose (table sugar) 97.0 97.0 48.5
Maple sugar 85.2 4.3 4.3 75.0 41.8
Honey 81.9 33.8 42.4 1.5 4.2 43.2
High fructose corn syrup (42%) 71.0 36.9 29.8 2.1 29.8
High fructose corn syrup (55%) 77.0 30.8 42.4 2.3 42.4
High fructose corn syrup (90%) 80.0 7.2 72 72.0
Molasses 60.0 11.2 12.9 34.7 30.3
Sorghum syrup 65.7 33.5
Brown sugar 89.7 5.2 84.1 42.1
M & M chocolate candy 64.7 54.9 7.6 27.5
Lifesavers 66.5 66.5 33.3
Hard candy 62.3 66.7 33.4
Bit O Honey 42.4 5.0 0.5 27.0 2.5 5.0 14.0
Almond Joy 44.9
Baby Ruth 42.0
Butterfinger 48.8
Caramello Candy Bar 54.2
Nestles Crunch Candy Bar 52.4 0.2 45.1 6.8 22.8
Nestles 100 Grand Candy Bar 63.5
Nestles Raisinets 62.5
Reeses Pieces 50.0
Skittles 76.4
Nestles Plain Milk Chocolate Candy Bar 51.0
Hershey’s Kisses 50.0
Sugar babies 72.9
Milk Duds 50.0
Junior Mints 82.2

Source:   Dr. Loren Cordain

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How much sugar should I eat each day?

Sugar is all empty calories with no nutritional value.Sugar is all empty calories with no nutritional value.

The USDA suggests that you get about half of your calories from carbohydrates. The sugar found naturally in fruit and vegetables is OK because the fruits or vegetables add a lot of good nutrition. Sugar from corn syrup or table sugar should really be used sparingly because it adds no nutritional value, just empty calories.The USDA suggests that the amount of added sugar calories (the sugar not found naturally in the fruits or vegetables you eat) should fit into your body. Your daily discretionary calories is the number of calories you can eat each day over the amount you need nutritionally and not gain weight. For most of us, that discretionary calorie budget is around 100 to 300 calories per day.You need a certain number of calories to keep your body functioning and provide energy for physical activities. Think of the calories you need for energy like money you have to spend.  Each person has a total calorie “budget.”  This budget can be divided into “essentials” and “extras.”

With a financial budget, the essentials are items like rent and food.  The extras are things like movies and vacations.  In a calorie budget, the “essentials” are the minimum calories required to meet your nutrient needs.  By selecting the lowest fat and no-sugar-added forms of foods in each food group you would make the best nutrient “buys.”  Depending on the foods you choose, you may be able to spend more calories than the amount required to meet your nutrient needs.  These calories are the “extras” that can be used on luxuries like solid fats, added sugars, and alcohol, or on more food from any food group.  They are your “discretionary calories.”

Each person has an allowance for some discretionary calories.  But, many people have used up this allowance before lunch-time!  Most discretionary calorie allowances are very small, between 100 and 300 calories, especially for those who are not physically active.  For many people, the discretionary calorie allowance is totally used by the foods they choose in each food group, such as higher fat meats, cheeses, whole milk, or sweetened bakery products.

You can use your discretionary calorie allowance to:

  • Eat more foods from any food group than the food guide recommends.
  • Eat higher calorie forms of foods—those that contain solid fats or added sugars.  Examples are whole milk, cheese, sausage, biscuits, sweetened cereal, and sweetened yogurt.
  • Add fats or sweeteners to foods.  Examples are sauces, salad dressings, sugar, syrup, and butter.
  • Eat or drink items that are mostly fats, caloric sweeteners, and/or alcohol, such as candy, soda, wine, and beer.

For example, assume your calorie budget is 2,000 calories per day.  Of these calories, you need to spend at least 1,735 calories for essential nutrients, if you choose foods without added fat and sugar.  Then you have 265 discretionary calories left.  You may use these on “luxury” versions of the foods in each group, such as higher fat meat or sweetened cereal.  Or, you can spend them on sweets, sauces, or beverages.  Many people overspend their discretionary calorie allowance, choosing more added fats, sugars, and alcohol than their budget allows.

12 teaspoons added sugar for a 2000 calorie per day diet

No more than 40 grams per day for a 2000 calorie diet.
Remember that the daily limit of 40 grams refers to refined/processed sugars only. There seems to be no limit on natural sugars, however. So, if it’s fruits and sugar cane, for which, you’re craving, sweet deal.

How many grams of sugar are appropriate per day for the average adult?

There is no definitive answer to the question, but 40 grams is the recommended amount for non-diabetic people. If you’re diabetic or borderline diabetic, please see the note at the bottom. 40 grams of sugar refers mainly to added sugar, which is anything that is put into foods rather that which is naturally occurring such as in fruit. By this logic, for instance, ALL sugar in soda would be considered “added,” since the beverage itself is constructed rather than harvested.

More input from WikiAnswers contributors:

Actually, this is a bit of a complicated question. Carbohydrates can take the form of sugar once digested, and a certain amount of sugar, as the answer above indicates, occurs naturally in food. However, the following bit from, I found helpful: “In petitioning for labeling changes regarding sugar, CSPI (Center for Science in the Public Interest), joined by dozens of leading health experts, also wants the FDA to set a maximum recommended daily intake (Daily Value) for added sugars of 10 teaspoons (40 grams) and require labels to disclose the percentage of the Daily Value a food provides.”There are many naturally occurring sugars such as sucrose which is a combination of glucose and fructose (or fruit sugar), lactose (from milk), maltose and galactose. You don’t want too many of the simple sugar glucose, but you can have a few more of the complex ones. If you digest too many simple sugars, your body gets swamped and the excess that is not used by your body gets stored as fat. Also useful to know is that sugars also enters your cells using the same pathway as Vitamin C – so, too much sugar and your body does not absorb Vitamin C as well. Too much sugar also interrupts your immune system. However, you can eat or drink natural sugars in moderation – say up to 100 grams a day (like orange juice which contains quite a lot of fructose).

From a health standpoint, specifically adding simple table sugar is a favorable alternative to adding a potentially hazardous substance such as high fructose corn syrup. This isn’t to say sugar itself lacks dietary benefits. Sugar, in its original state, is a naturally produced substance rich in vitamins and minerals. And if refined properly, retains these qualities (so long as it remains in the form of table sugar.) In addition, a regular intake of table sugar is important in regulating insulin productivity. There are also positive metabolic effects. Sugar is added to FDA-approved energy products for a reason–it’s a safe stimulant that augments energy in a confined period of time and promotes a heart-healthy agenda. Thusly, it is somewhat difficult to say exactly how much sugar per day any one person may require. For someone with a regular metabolism, that doesn’t devote time to exercise, a 100g maximum should not be crossed (and in many cases not be approached.) However, athletes may consume 150% of this without seeing notable side-effects. It is important that I reiterate that in either case this threshold should not be approached. Sugar in very high doses is dangerous; if you’re concerned for your health it is best to stay at a far more shallow intake than the maximum dosage recommends.

Amount of any food per day is always subjective to the following:

a. Age
b. Health conditions
c. Physical activity(calorie expenditure per day)
d. General food habits(based on locality of individual, he may be consuming more of one food and may be immune to bad effects of it)
e. Others
There are many other minor factors which may determine the amount of sugars that a person needs. So based on the law of individualism, each individual is unique and their needs are different based on various factors.

Processed sugar is not necessary at all in anyone’s daily diet. It should be avoided. Our body gets enough carbohydrates from ordinary foods and converts raw carbs to sugars as needed. Grains, fruits, and other carbs provide enough(sometimes too much) sugars as is. Dried fruits such as rasins are especially full of sugars. To add even more processed sugar is harmful. As a dentist, I see daily the harm done by hard candy, chocolate, soda, cough drops (98% sugar), sweetened tea, coffee (with either sugar and sometimes powdered cream substitute (contains high % sugar), pastries, pies, cakes, cookies. NONE OF THESE FOODS ARE NECESSARY AND SHOULD BE AVOIDED UNLESS IT IS A RARE SPECIAL OCCASION. Even worse, many of our schools support certain school programs by selling candy, having soda machines in the schools, having juice machines in the schools (just as harmful as soda), and letting teachers give out candy as a reward to children. If schools found out that something that they served in the cafeteria caused a child’s toe to fall off occasionally, I bet they would quit serving what caused the toe to fall off. Am I right?? Well, in the same respect, how can schools allow processed sugars, which cause teeth rot and fall out or have to be pulled, to be served in their institution. How can they allow a teacher to award a kid with a substance that is known by EVERYONE to cause tooth decay??? Hope I have been of some help to you. Consult a dietitian if you disagree with anything that I have said.


The answer is different for each individual. A much more useful answer that may save lives is: Everyone is different. If you are diabetic and worried about harming your body with sugar intake (as you should be), then it is small comfort if your intake is fine for average people but tends to cause high blood sugar for *you* in particular.

Rather than researching grams of sugar and asking people (or even doctors) if that’s harmful, you should buy a glucometer (blood glucose meter) at any drugstore, learn to use it, and find out what foods you can eat (on your current medicine and diet) that will keep your blood sugar in the safe ranges according to the link below “How to keep your blood sugar under control”.

  • Fasting blood sugar under 100 mg/dl (5.5 mmol/L)
  • One hour after meals under 140 mg/dl (7.8 mmol/L)
  • Two hours after meals under 120 mg/dl (6.6 mmol/L)

After you have determined how much milk or sugar or carbohydrate you can eat and stay within these boundaries, then and only then are absolute grams of carbohydrate or sugar a useful thing to know.

The Bittersweet Truth About Sugar

We love it; in fact, we’re born loving it, and the taste for sugar never seems to go away. But if you’ve been noticing that more and more people are discussing the evils of sugar, you’ve probably discovered that, like many delightful things in life, a little sugar is a good thing, but a lot of sugar can be very, very bad. Sugar, we’re told, makes us fat, leads us into diabetes and creates cravings we can’t live without. Avoidance of all sugar (including the natural sugars found in fruits) has formed the basis of some of the latest diets, helping people lose weight for a time, but often resulting in ling term crankiness and sometimes even constipation. Do we need sugar? How much is too much?

Beauty Tips Girl Friday

There’s no established RDA (Recommended Daily Allowance) for sugar, because as far as it’s known, we don’t need sugar for nutrition. All foods have some natural sugars, but sugar itself—the white or brown stuff we put in our cookies, is a purely optional taste sensation. The USDA (United States Department of Agriculture) recommends that sugar make up no more than 8% of the daily intake of calories, but most American adults take in twice that much. It’s an easy thing to do when a single can of soda pop contains more than 10 teaspoons of sugar!

Sugar isn’t good for you, but it tastes so good that even people who have been warned away from it for their very lives sometimes “cheat” anyway. For the rest of us, sugar is an enduring passion, and one we occasionally monitor and regulate, especially as we put on weight or grow into the age range where our doctors are worrying us about diabetes. So, what are the best ways to put a temporary restraining order on the vast amounts of sugar most of us regularly consume?

  1. Think about it. Most people don’t have any idea of their sugar intake. Who has time to read the labels on spaghetti sauce, pudding, fruit filled yogurt or our favorite Starbucks libations? When you do, you may be shocked to find sugar—and lots of it—in baby formulas, “healthy” cereals and nearly any prepackaged food you can name. Try this: read all the labels in your kitchen as you take things out to cook or eat, and make a note of the ones that don’t contain sugar. You may find it’s a short list.
  2. Kill the soda machine. Soda pop is a huge culprit in the sugar wars. A 12 ounce can of Dr. Pepper has 38 grams of sugar and 140 calories. If you gave up one daily can of soda, you’d save 980 calories a week, and at the end of a month, will have saved over 3,500 calories, or one pound of weight. The worst thing about soda is that there are no nutrients in it, so it doesn’t really solve the problem of hunger. The water in a soda is so saturated with sugar that it actually creates an additional need in the body for water, so it also doesn’t solve the problem of thirst. If you find you really love the bubbly, cold aspect of soda, switch to club soda or seltzer, both of which are sugar free.
  3. Cut the sugar cravings. Head them off at the pass by eating real foods containing complex carbohydrates such as whole grains, proteins from meat, eggs and cheese and fiber found in vegetables. Try substituting a handful of almonds for a bag of M&Ms : you’ll get protein and fiber that will ease your hunger and last awhile.
  4. Eat low-sugar sweets. Who says you should give up chocolate? In fact, dark chocolate contains healthy components; anti-oxidants shown to prevent cancer, enhance well-being and satiate hunger. But buy the good stuff; the dark chocolate whose ingredients include cocoa mass, cocoa liquor, sugar (yes, sugar) and lecithin. Don’t buy chocolate whose first ingredient is sugar; it’s been so watered down by the cheap addition of white sugar that its natural benefits are annulled.

The Facts on Fiber

If we all eat twice as much sugar as we should, we also eat about half as much fiber as we need. The ADA (American Dietetic Association) recommends we eat 20-35 grams of fiber each day. But why is fiber necessary? And how can we get more of it?

Beauty Tips Girl Friday
  1. What is fiber? Fiber is plant material that, rather than being digested, moves through the intestinal tract. You can find fiber in vegetables, grains and fruits. What’s it good for? Fiber keeps you regular, which is why it’s the main ingredient in natural laxatives. Fiber takes action on the bowels and has also been shown to lower cholesterol in the blood by binding with it in the digestive system and passing it out of the body as waste. Fiber has been shown to help prevent colon cancer, diseases of the intestinal tract and heart disease. Another thing fiber prevents is hunger: eating foods rich in fiber makes you feel fuller, and prevents overeating.
  2. Can you get too much fiber? Yes indeed! But usually it’s from overdoing the laxatives or eating too much high-fiber cereal. Eating too much fiber can cause bloating and give you diarrhea, but on the bright side, it’s tough enough to get a lot of fiber that most people never get too much. Some eating disordered folks have ridden the fiber train in an effort to lose weight, which can interfere with your body absorbing minerals it needs to stay healthy. But most people don’t get nearly the fiber they need to maximize their health.
  3. Does fiber break down if I cook my veggies mushy? Nope. Fiber doesn’t cook away like water does, so you can boil those carrots all day if you want.
  4. What else should I do when I eat fiber? Drink lots of water. Keep that fiber progressing through your intestines by lubricating them with plenty of water, or you may wind up …bound up.
  5. Isn’t fiber just for old people? Those are the ones eating fiber rich cereals in the TV ads. Actually everyone needs fiber, and with today’s school lunches, it’s going to be a challenge to make sure your kids get enough fiber in their other meals. Try to brainwash your little darlings into loving fresh fruits and veggies, and don’t let them torture you with guilt when you refuse to take them out for a McNasty Meal. Parents need fiber too: it’s easy to get sluggish if you’re living on coffee and breakfast bars: get yourself some fine flaxseed based cereals and wake up your colon a couple of times a week. Raisin Bran is one popular cereal whose basis is practically pure fiber.
  6. Where can I find fiber? You can find fiber in all the things you probably don’t eat because they’re “boring”. Beans, peas and lentils are fantastically rich in fiber; brown rice, oats. barley and other whole grains have a lot of fiber, too. But don’t expect to get much fiber from white rice: the brown husk that comes with the natural rice has been rubbed off, and with it, much of the accompanying fiber. Fruits and veggies have some fiber, but a serving of fruit will give you about two grams of fiber, whereas a serving of kidney beans will give you six times that much.
  7. I want more fiber! What should I do? Eat canned beans, which are easy to heat and serve (and really delicious if you bake them with molasses, onions and bacon). Skip the ultra-sweet cereals and eat oatmeal, add bran cereal to your yogurt. Eat real food: junk food usually has the fiber removed to make way for sugar, starch and chemicals. Go for apples, pears, nuts and broccoli. You won’t find fiber in booze, ice
Source: Dr. Loren Cordain

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