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D-Fructose
D-Fructofuranose
D-Fructofuranose
Names
IUPAC name
Fructose
Other names
fruit sugar,[1] levulose,[2] D-fructofuranose, D-fructose, D-arabino-hexulose
Identifiers
3D model (JSmol)
ChEMBL
ChemSpider
ECHA InfoCard 100.000.303 Edit this at Wikidata
KEGG
UNII
  • InChI=1S/C6H12O6/c7-1-3-4(9)5(10)6(11,2-8)12-3/h3-5,7-11H,1-2H2/t3-,4-,5+,6-/m1/s1 checkY
    Key: RFSUNEUAIZKAJO-ARQDHWQXSA-N checkY
  • InChI=1/C6H12O6/c7-1-3-4(9)5(10)6(11,2-8)12-3/h3-5,7-11H,1-2H2/t3-,4-,5+,6-/m1/s1
    Key: RFSUNEUAIZKAJO-ARQDHWQXBD
  • O[C@H]1[C@H](O)[C@H](O[C@]1(O)CO)CO
Properties
C6H12O6
Molar mass 180.16 g/mol
Melting point 103 °C
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
checkY verify (what is checkY☒N ?)

Fructose, or fruit sugar, is a simple monosaccharide found in many foods. It is one of the three important dietary monosaccharides along with glucose and galactose. The organic fructose molecule was first discovered by Augustin-Pierre Dubrunfaut in 1847.[3] Fructose is a white solid that dissolves in water – it is the most water-soluble of all the sugars.[4] Honey, tree fruits, berries, melons, and some root vegetables contain significant amounts of molecular fructose, usually in combination with glucose, stored in the form of sucrose. About 240,000 tonnes of crystalline fructose are produced annually.[5]

Fructose is a component of sucrose. Sucrose is a disaccharide derived from the condensation of glucose and fructose. Fructose is derived from the digestion of table sugar (sucrose).

Crystalline fructose and high-fructose corn syrup are often confused as the same product. Crystalline fructose, which is often produced from a fructose-enriched corn syrup, is indeed the monosaccharide. High-fructose corn syrup, however, refers to a family of mixtures of varying amounts of fructose and glucose.

Chemical properties

Figure 1: Relationship between the acyclic and the cyclic (hemiketal) isomers of fructose.
d- and l-isomers of fructose (open-chain form)

Fructose is a 6-carbon polyhydroxyketone. It is an isomer of glucose, i.e. both have the same molecular formula (C6H12O6) but they differ structurally. Crystalline fructose adopts a cyclic six-membered structure owing to the stability of its hemiketal and internal hydrogen-bonding. This form is formally called D-fructopyranose. In solution, fructose exists as an equilibrium mixture of 70% fructopyranose and about 22% fructofuranose, as well as small amounts of three other forms, including the acylic structure.[6]

Reactions

Fructose and fermentation

Fructose may be anaerobically fermented by yeast or bacteria.[7] Yeast enzymes convert sugar (glucose, or fructose) to ethanol and carbon dioxide. The carbon dioxide released during fermentation will remain dissolved in water where it will reach equilibrium with carbonic acid unless the fermentation chamber is left open to the air. The dissolved carbon dioxide and carbonic acid produce the carbonation in bottle fermented beverages.[8]

Fructose and Maillard reaction

Fructose undergoes the Maillard reaction, non-enzymatic browning, with amino acids. Because fructose exists to a greater extent in the open-chain form than does glucose, the initial stages of the Maillard reaction occurs more rapidly than with glucose. Therefore, fructose potentially may contribute to changes in food palatability, as well as other nutritional effects, such as excessive browning, volume and tenderness reduction during cake preparation, and formation of mutagenic compounds.[9]

Dehydration

Fructose readily dehydrates to give hydroxymethylfurfural ("HMF"). This process may in the future be part of a low-cost, carbon-neutral system to produce replacements for petrol and diesel from plantations.[10]

Physical and functional properties

Relative sweetness

The primary reason that fructose is used commercially in foods and beverages, besides its low cost, is its high relative sweetness. It is the sweetest of all naturally occurring carbohydrates. Fructose is generally regarded as being 1.73 times as sweet as sucrose.[11][12] However, it is the 5-ring form of fructose that is sweeter; the 6-ring form tastes about the same as usual table sugar. Warming fructose leads to formation of the 6-ring form.[13]

Figure 2: Relative sweetness of sugars and sweeteners.

The sweetness of fructose is perceived earlier than that of sucrose or dextrose, and the taste sensation reaches a peak (higher than sucrose) and diminishes more quickly than sucrose. Fructose can also enhance other flavors in the system.[11]

Sweetness synergy

Fructose exhibits a sweetness synergy effect when used in combination with other sweeteners. The relative sweetness of fructose blended with sucrose, aspartame, or saccharin is perceived to be greater than the sweetness calculated from individual components.[14]

Fructose solubility and crystallization

Fructose has higher solubility than other sugars as well as other sugar alcohols. Fructose is therefore difficult to crystallize from an aqueous solution.[11] Sugar mixes containing fructose, such as candies, are softer than those containing other sugars because of the greater solubility of fructose.[15]

Fructose hygroscopicity and humectancy

Fructose is quicker to absorb moisture and slower to release it to the environment than sucrose, dextrose, or other nutritive sweeteners.[14] Fructose is an excellent humectant and retains moisture for a long period of time even at low relative humidity (RH). Therefore, fructose can contribute to improved quality, better texture, and longer shelf life to the food products in which it is used.[11]

Freezing point

Fructose has a greater effect on freezing point depression than disaccharides or oligosaccharides, which may protect the integrity of cell walls of fruit by reducing ice crystal formation. However, this characteristic may be undesirable in soft-serve or hard-frozen dairy desserts.[11]

Fructose and starch functionality in food systems

Fructose increases starch viscosity more rapidly and achieves a higher final viscosity than sucrose because fructose lowers the temperature required during gelatinizing of starch, causing a greater final viscosity.[16]

Food sources

Natural sources of fructose include fruits, vegetables (including sugar cane), and honey.[17] Fructose is often further concentrated from these sources. The highest dietary sources of fructose, besides pure crystalline fructose, are foods containing table sugar (sucrose), high-fructose corn syrup, agave nectar, honey, molasses, maple syrup, and fruit juices, as these have the highest percentages of fructose (including fructose in sucrose) per serving compared to other common foods and ingredients. Fructose exists in foods either as a free monosaccharide, or bound to glucose as sucrose, a disaccharide. Fructose, glucose, and sucrose may all be present in a food; however, different foods will have varying levels of each of these three sugars.

The sugar contents of common fruits and vegetables are presented in Table 1. In general, in foods that contain free fructose, the ratio of fructose to glucose is approximately 1:1; that is, foods with fructose usually contain about an equal amount of free glucose. A value that is above 1 indicates a higher proportion of fructose to glucose, and below 1, a lower proportion. Some fruits have larger proportions of fructose to glucose compared to others. For example, apples and pears contain more than twice as much free fructose as glucose, while for apricots the proportion is less than half as much fructose as glucose.

Apple and pear juices are of particular interest to pediatricians because the high concentrations of free fructose in these juices can cause diarrhea in children. The cells (enterocytes) that line children's small intestines have less affinity for fructose absorption than for glucose and sucrose.[18] Unabsorbed fructose creates higher osmolarity in the small intestine, which draws water into the gastrointestinal tract, resulting in osmotic diarrhea. This phenomenon is discussed in greater detail in the Health Effects section.

Table 1 also shows the amount of sucrose found in common fruits and vegetables. Sugar cane and sugar beet have a high concentration of sucrose, and are used for commercial preparation of pure sucrose. Extracted cane or beet juice is clarified, removing impurities; and concentrated by removing excess water. The end product is 99.9% pure sucrose. Sucrose-containing sugars include common table white granulated sugar and powdered sugar, as well as brown sugar.[19]

Table 1. Sugar content of selected common plant foods (g/100g)
Food Item Total
Carbohydrate
 Total
Sugars 		Free
Fructose 		Free
Glucose 		Sucrose Fructose/
Glucose
Ratio 		Sucrose
as a % of
Total Sugars
Fruits              
Apple 13.8 10.4 5.9 2.4 2.1 2.0 19.9
Apricot 11.1 9.2 0.9 2.4 5.9 0.7 63.5
Banana 22.8 12.2 4.9 5.0 2.4 1.0 20.0
Fig, dried 63.9 47.9 22.9 24.8 0.07 0.93 0.001
Grapes 18.1 15.5 8.1 7.2 0.2 1.1 1.0
Peach 9.5 8.4 1.5 2.0 4.8 0.9 56.7
Pear 15.5 9.8 6.2 2.8 0.8 2.1 8.0
Pineapple 13.1 9.9 2.1 1.7 6.0 1.1 60.8
Plum 11.4 9.9 3.1 5.1 1.6 0.66 0.16
Vegetables              
Beet, Red 9.6 6.8 0.1 0.1 6.5 1.0 96.2
Carrot 9.6 4.7 0.6 0.6 3.6 1.0 70.0
Corn, Sweet 19.0 3.2 0.5 0.5 2.1 1.0 64.0
Red Pepper, Sweet 6.0 4.2 2.3 1.9 0.0 1.2 0.0
Onion, Sweet 7.6 5.0 2.0 2.3 0.7 0.9 14.3
Sweet Potato 20.1 4.2 0.7 1.0 2.5 0.9 60.3
Yam 27.9 0.5 tr tr tr na tr
Sugar Cane 13 - 18 0.2 – 1.0 0.2 – 1.0 11 - 16 1.0 100
Sugar Beet 17 - 18 0.1 – 0.5 0.1 – 0.5 16 - 17 1.0 100

Data obtained at [3].[20] All data with a unit of g (gram) are based on 100 g of a food item. The fructose / glucose ratio is calculated by dividing the sum of free fructose plus half sucrose by the sum of free glucose plus half sucrose.

Fructose is also found in the synthetically manufactured sweetener, high-fructose corn syrup (HFCS). Hydrolyzed corn starch is used as the raw material for production of HFCS. Through the enzymatic treatment, glucose molecules are converted into fructose.[19] There are three types of HFCS, each with a different proportion of fructose: HFCS-42, HFCS-55, and HFCS-90. The number for each HFCS corresponds to the percentage of synthesized fructose present in the syrup. HFCS-90 has the highest concentration of fructose, and is typically used to manufacture HFCS-55; HFCS-55 is used as sweetener in soft drinks, while HFCS-42 is used in many processed foods and baked goods.

Carbohydrate content of commercial sweeteners (percent)

Sugar Fructose Glucose Sucrose (Fructose-Glucose) Other Sugars
Granulated Sugar 0 0 100 0
Brown Sugar 1 1 97 1
HFCS-42 42 53 0 5
HFCS-55 55 41 0 4
HFCS-90 90 5 0 5
Honey 50 44 1 5
Maple Syrup 1 4 95 0
Molasses 23 21 53 3
Corn Syrup 0 35 0 0

Data obtained from Kretchmer, N. & Hollenbeck, CB (1991). Sugars and Sweeteners, Boca Raton, FL: CRC Press, Inc.[19] for HFCS, and USDA for fruits and vegetables and the other refined sugars.[20]

Cane and beet sugars have been used as the major sweetener in food manufacturing for centuries. However, with the development of HFCS, a significant shift occurred in the type of sweetener consumption. As seen in Figure 3, this change happened in the 1970s. Contrary to the popular belief, however, with the increase of HFCS consumption, the total fructose intake has not dramatically changed. Granulated sugar is 99.9% pure sucrose, which means that it has equal ratio of fructose to glucose. The most commonly used forms of HFCS, HFCS-42 and HFCS-55, have a roughly equal ratio of fructose to glucose, with minor differences. HFCS has simply replaced sucrose as a sweetener. Therefore, despite the changes in the sweetener consumption, the ratio of glucose to fructose intake has remained relatively constant.[21]

Figure 3: Adjusted consumption of refined sugar per capita in the U.S.

Fructose digestion and absorption in humans

Fructose exists in foods as either a monosaccharide (free fructose) or as a unit of a disaccharide (sucrose). Free fructose is absorbed directly by the intestine; however, when fructose is consumed in the form of sucrose, digestion occurs entirely in the upper small intestine. As sucrose comes into contact with the membrane of the small intestine, the enzyme sucrase catalyzes the cleavage of sucrose to yield one glucose unit and one fructose unit. Fructose is absorbed in the small intestine, then enters the hepatic portal vein and is directed toward the liver.

Figure 4: Hydrolysis of sucrose to glucose and fructose by sucrase.

The mechanism of fructose absorption in the small intestine is not completely understood. Some evidence suggests active transport, because fructose uptake has been shown to occur against a concentration gradient.[22] However, the majority of research supports the claim that fructose absorption occurs on the mucosal membrane via facilitated transport involving GLUT5 transport proteins. Since the concentration of fructose is higher in the lumen, fructose is able to flow down a concentration gradient into the enterocytes, assisted by transport proteins. Fructose may be transported out of the enterocyte across the basolateral membrane by either GLUT2 or GLUT5, although the GLUT2 transporter has a greater capacity for transporting fructose and therefore the majority of fructose is transported out of the enterocyte through GLUT2.

Figure 5: Intestinal sugar transport proteins.

Capacity and rate of absorption

The absorption capacity for fructose in monosaccharide form ranges from less than 5 g to 50 g and adapts with changes in dietary fructose intake. Studies show the greatest absorption rate occurs when glucose and fructose are administered in equal quantities.[23] When fructose is ingested as part of the disaccharide sucrose, absorption capacity is much higher because fructose exists in a 1:1 ratio with glucose. It appears that the GLUT5 transfer rate may be saturated at low levels, and absorption is increased through joint absorption with glucose.[24] One proposed mechanism for this phenomenon is a glucose-dependent cotransport of fructose. In addition, fructose transfer activity increases with dietary fructose intake. The presence of fructose in the lumen causes increased mRNA transcription of GLUT5, leading to increased transport proteins. High-fructose diets[vague] have been shown to increase abundance of transport proteins within 3 days of intake.[25]

Malabsorption

Main article: Fructose malabsorption

Several studies have measured the intestinal absorption of fructose using hydrogen breath test.[26][27][28][29] These studies indicate that fructose is not completely absorbed in the small intestine. When fructose is not absorbed in the small intestine, it is transported into the large intestine, where it is fermented by the colonic flora. Hydrogen is produced during the fermentation process and dissolves into the blood of the portal vein. This hydrogen is transported to the lungs, where it is exchanged across the lungs and is measurable by the hydrogen breath test. The colonic flora also produces carbon dioxide, short-chain fatty acids, organic acids, and trace gases in the presence of unabsorbed fructose.[30] The presence of gases and organic acids in the large intestine causes gastrointestinal symptoms such as bloating, diarrhea, flatulence, and gastrointestial pain [26] Exercise immediately after consumption can exacerbate these symptoms by decreasing transit time in the small intestine, resulting in a greater amount of fructose being emptied into the large intestine.[31]

Fructose metabolism

All three dietary monosaccharides are transported into the liver by the GLUT 2 transporter.[32] Fructose and galactose are phosphorylated in the liver by fructokinase (Km= 0.5 mM) and galactokinase (Km = 0.8 mM). By contrast, glucose tends to pass through the liver (Km of hepatic glucokinase = 10 mM) and can be metabolised anywhere in the body. Uptake of fructose by the liver is not regulated by insulin.

Fructolysis

Fructolysis initially produces fructose 1,6-bisphosphate, which is split with aldolase to produce phosphate derivatives of the trioses dihydroxyacetone (dihydroxyacetone phosphate) and glyceraldehyde (glyceraldehyde 3-phosphate).[4] These are then metabolized either in the gluconeogenic pathway for glycogen replenishment and/or complete metabolism in the fructolytic pathway to pyruvate, which after conversion to acetyl-CoA enters the Krebs cycle, and is converted to citrate and subsequently directed toward ’’de novo’’ synthesis of the free fatty acid palmitate.[33]

Metabolism of fructose to DHAP and glyceraldehyde

The first step in the metabolism of fructose is the phosphorylation of fructose to fructose 1-phosphate by fructokinase, thus trapping fructose for metabolism in the liver. Fructose 1-phosphate then undergoes hydrolysis by aldolase B to form DHAP and glyceraldehydes; DHAP can either be isomerized to glyceraldehyde 3-phosphate by triosephosphate isomerase or undergo reduction to glycerol 3-phosphate by glycerol 3-phosphate dehydrogenase. The glyceraldehyde produced may also be converted to glyceraldehyde 3-phosphate by glyceraldehyde kinase or converted to glycerol 3-phosphate by glyceraldehyde 3-phosphate dehydrogenase. The metabolism of fructose at this point yields intermediates in the gluconeogenic and fructolytic pathways leading to glycogen synthesis as well as fatty acid and triglyceride synthesis.

Synthesis of glycogen from DHAP and glyceraldehyde 3 phosphate

The resultant glyceraldehyde formed by aldolase B then undergoes phosphorylation to glyceraldehyde 3-phosphate. Increased concentrations of DHAP and glyceraldehyde 3-phosphate in the liver drive the gluconeogenic pathway toward glucose and subsequent glycogen synthesis.[34] It appears that fructose is a better substrate for glycogen synthesis than glucose and that glycogen replenishment takes precedence over triglyceride formation.[citation needed] Once liver glycogen is replenished, the intermediates of fructose metabolism are primarily directed toward triglyceride synthesis.[citation needed]

Figure 6: Metabolic conversion of fructose to glycogen in the liver.

Synthesis of triglyceride from DHAP and glyceraldehyde 3 phosphate

Carbons from dietary fructose are found in both the free fatty acid and glycerol moieties of plasma triglycerides. High fructose consumption can lead to excess pyruvate production, causing a buildup of Krebs cycle intermediates.[33] Accumulated citrate can be transported from the mitochondria into the cytosol of hepatocytes, converted to acetyl CoA by citrate lyase and directed toward fatty acid synthesis.[33][35] Additionally, DHAP can be converted to glycerol 3-phosphate as previously mentioned, providing the glycerol backbone for the triglyceride molecule.[35] Triglycerides are incorporated into very low density lipoproteins (VLDL), which are released from the liver destined toward peripheral tissues for storage in both fat and muscle cells.

Figure 7: Metabolic conversion of fructose to triglyceride in the liver.

Health effects

Digestive problems

Fructose absorption occurs via the GLUT-5[36] (fructose only) transporter, and the GLUT2 transporter, for which it competes with glucose and galactose. A deficiency of GLUT 5 may result in excess fructose carried into the lower intestine.[citation needed] There, it can provide nutrients for the existing gut flora, which produce gas. It may also cause water retention in the intestine. These effects may lead to bloating, excessive flatulence, loose stools, and even diarrhea depending on the amounts eaten and other factors. For some people, fructose malabsorption may be a major health concern.

Metabolic syndrome

Excess fructose consumption has been hypothesized to be a cause of insulin resistance, obesity,[37] elevated LDL cholesterol and triglycerides, leading to metabolic syndrome.[38] Fructose consumption has been shown to be correlated with obesity,[39][40] especially central obesity which is thought to be the most dangerous kind of obesity. A study in mice showed that a high fructose intake increases adiposity.[41]

Although all simple sugars have nearly identical chemical formulae, each has distinct chemical properties. This can be illustrated with pure fructose. A journal article reports that, "...fructose given alone increased the blood glucose almost as much as a similar amount of glucose (78% of the glucose-alone area)".[42][43][44][44][45]

One study concluded that fructose "produced significantly higher fasting plasma triacylglycerol values than did the glucose diet in men" and "...if plasma triacylglycerols are a risk factor for cardiovascular disease, then diets high in fructose may be undesirable".[46] Bantle et al. "noted the same effects in a study of 14 healthy volunteers who sequentially ate a high-fructose diet and one almost devoid of the sugar."[47]

Fructose is a reducing sugar, as are all monosaccharides. The spontaneous chemical reaction of simple sugar molecules binding to proteins, known as glycation, is thought to be a significant cause of damage in diabetics. Fructose appears to be equivalent to glucose in this regard and so does not seem to be a better answer for diabetes for this reason alone, save for the smaller quantities required to achieve equivalent sweetness in some foods.[48] This may be an important contribution to senescence and many age-related chronic diseases.[49]

Compared to sucrose

Studies that have compared high-fructose corn syrup (an ingredient in nearly all soft drinks sold in the US) to sucrose (common table sugar) find that most measured physiological effects are equivalent. For instance, Melanson et al. (2006), studied the effects of HFCS and sucrose sweetened drinks on blood glucose, insulin, leptin, and ghrelin levels. They found no significant differences in any of these parameters.[50] This is not surprising, since sucrose is a disaccharide that digests to 50% fructose and 50% glucose, whereas the high-fructose corn syrup most commonly used on soft drinks is 55% fructose and 45% glucose. The difference between the two lies in the fact that HFCS contains little sucrose, the fructose and glucose being independent moieties.

Fructose is often recommended for diabetics because it does not trigger the production of insulin by pancreatic β cells, probably because β cells have low levels of GLUT5.[51][52][53] Fructose has a very low glycemic index of 19 ± 2, compared with 100 for glucose and 68 ± 5 for sucrose.[54] Fructose is also seventy-three percent sweeter than sucrose (see 2.1 Relative Sweetness) at room temperature, so diabetics can use less of it. Studies show that fructose consumed before a meal may even lessen the glycemic response of the meal.[55] Its sweetness changes at higher temperatures, so its effects in recipes are not equivalent to those of sucrose (i.e., table sugar).[citation needed]

Liver disease

"The medical profession thinks fructose is better for diabetics than sugar," says Meira Field, Ph.D., a research chemist at United States Department of Agriculture, "but every cell in the body can metabolize glucose. However, all fructose must be metabolized in the liver. The livers of the rats on the high fructose diet looked like the livers of alcoholics, plugged with fat and cirrhotic."[56] While a few other tissues (e.g., sperm cells[57] and some intestinal cells) do use fructose directly, fructose is almost entirely metabolized in the liver.[56]

"When fructose reaches the liver," says Dr. William J. Whelan, a biochemist at the University of Miami School of Medicine, "the liver goes bananas and stops everything else to metabolize the fructose." Eating fructose instead of glucose results in lower circulating insulin and leptin levels, and higher ghrelin levels after the meal.[58] Since leptin and insulin decrease appetite and ghrelin increases appetite, some researchers suspect that eating large amounts of fructose increases the likelihood of weight gain.[59]

Excessive fructose consumption is also believed to contribute to the development of non-alcoholic fatty liver disease.[60]

Gout

It has been suggested in a recent British Medical Journal study that high consumption of fructose is linked to gout. Cases of gout have risen in recent years, despite commonly being thought of as a Victorian disease, and it is suspected that the fructose found in soft drinks (e.g., carbonated beverages) and other sweetened drinks is the reason for this.[61][62]

In order for the liver to process fructose, it must be phosphorylated by removal of phosphates from adenosine triphosphate (ATP). The ATP gets converted to adenosine monophosphate (AMP), then to inositol monophosphate (IMP), and finally to uric acid,[63] the agent in gout.

Glycemic index

Fructose has the lowest glycemic index (GI = 19) of all the natural sugars and may be used in moderation by diabetics. It is recommended that a maximum intake of 25g - 40g per day is adopted, provided that this is counted towards the daily calorie count. In comparison, ordinary table sugar (sucrose) has a GI of 65 and honey has a GI of 55. Fruit sugar has the advantage for diabetics that, being nearly twice as sweet as ordinary sugar if not heat-processed, the daily allowance can be stretched by using less for most applications. Many artificial sweeteners are not suitable for home-baking, but, with a little adjustment, many traditional recipes can be prepared using fructose.[64]

See also

References

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  2. ^ Levulose comes from the Latin word laevus, levo, "left side", levulose is the old word for the most occurring isomer of fructose. D-fructose rotate plane-polarised light to the left, hence the name.[1].
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