Fructose

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Fructose
Beta-D-Fructofuranose
IUPAC name (2R,3S,4R,5R)-2,5-Bis(hydroxymethyl)oxolane-2,3,4-triol
Other names D-arabino-Hexulose
Fruit sugar
beta-Levulose
Levulose
Identifiers
CAS number 53188-23-1 (D-fructose)
SMILES C(C1C(C(C(O1)(CO)O)O)O)O
Properties
Molecular formula C6H12O6
Molar mass 180.16 g mol−1
Melting point

β-D-fructose: 103°C
Except where noted otherwise, data are given for
materials in their standard state
(at 25 °C, 100 kPa)
Infobox disclaimer and references

Fructose (also levulose or laevulose) is a simple reducing sugar (monosaccharide) found in many foods and is one of the three important dietary monosaccharides along with glucose and galactose. Honey, tree fruits, berries, melons, and some root vegetables, such as beets, sweet potatoes, parsnips, and onions, contain fructose, usually in combination with sucrose and glucose. Fructose is also derived from the digestion of granulated table sugar (sucrose), a disaccharide consisting of glucose and fructose, and high-fructose corn syrup (HFCS).

Crystalline fructose and high-fructose corn syrup are often mistakenly confused as the same product. The former is simply pure (100%) fructose. The latter is composed of nearly equal amounts of fructose and glucose. Crystalline fructose is held to offer many unique benefits such as improved product texture, taste and stability. Specifically, when combined with other sweeteners and starches, crystalline fructose is said to boost cake height (in baked goods) and mouth-feel of foods and beverages and to produce a pleasing brown surface color and pleasant aroma when baking.[1]

Fructose is often recommended for, and consumed by, people with diabetes mellitus or hyperglycemia, because it does not raise blood glucose or insulin concentrations since it is metabolized without the need of insulin. However, this benefit is tempered by concern that fructose may have an adverse effect on plasma lipid and uric acid levels.

Contents

[edit] Chemical Properties

[edit] Classification and Structure

Fructose, also referred to as fruit sugar is a simple monosaccharide with a ketone functional group. Fructose is an isomer of glucose with the same empirical formula (C6H12O6) but with a different structure. Fructose is a 6-carbon polyhydroxyketone. Like glucose, it forms ring structures when dissolved in solution. When fructose forms a 5-member ring, the OH group on the fifth carbon atom attaches to the carbonyl group that is on the second carbon atom (D-Fructofuranose). Alternatively, the OH group on the sixth carbon may attach to the carbonyl carbon to form a 6-member ring (D-Fructopuranose). Fructose may be found at equilibrium containing a mixture of 70% fructopuranose and 30% fructofuranose [2]

Figure 1 Isomeric Forms of Fructose

[edit] Chemical Reactions

[edit] Fructose and Maillard Reaction

Fructose undergoes the Maillard reaction, non-enzymatic browning, with amino acids. Because of 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. [3]

[edit] Fructose and Fermentation

Fructose may be fermented by yeast or bacteria. [4] Yeast enzymes convert sugar (glucose, or fructose) to ethanol and carbon dioxide. Fermentation is accompanied by the release of carbon dioxide that causes foaming. [5] Colonic bacterial fermentation of fructose may cause gas, cramps, and diarrhea problems in people with fructose malabsorption. [6]

[edit] Physical and Functional Properties

[edit] Relative Sweetness

The primary reason that fructose is used commercially in foods and beverages is because of its relative sweetness.It is the sweetest of all naturally occurring carbohydrates. Fructose is 1.73 times sweeter than sucrose[7][8] .

Figure 2 Relative Sweetness of Sugars and Sweeteners

The Sweetness Intensity Profile of Fructose 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[9].

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[10].

[edit] Fructose Solubility and Crystallization

Compared to other sugars and sugar alcohols, fructose has the highest solubility. As a result, fructose is 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 [12].

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 [13]. 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 [14].

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[15].

[edit] 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].

[edit] Food Sources

The primary food sources of fructose are fruits, vegetables, and honey [17]. Fructose exists in foods either as a free monosaccharide or bound to glucose as the disaccharide, sucrose. Fructose, glucose, and sucrose can all be present in a food; however, different foods will have varying levels of each of these three sugars.

The sugar content of common fruits and vegetables are presented in Table 1. In general, foods that contain free fructose have equal amount of free glucose. In other words, the ratio of fructose to glucose roughly equals 1:1. A value that is above 1 indicates higher proportion of fructose to glucose and vice versa. Some of the 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 apricots contain less than a half of fructose than glucose.

Apple and pear juices are of particular interest to pediatricians due to the juices’ high concentration of free fructose relative to glucose, which can cause diarrhea in children. The cells of the small intestine, enterocytes, have lower affinity for fructose absorption compared with that 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 details in 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 juices are clarified from the impurities and concentrated by removing excess of water. The end product is 99.9% pure sucrose. Sucrose containing sugars include common white granulated sugar, powdered sugar, as well as brown sugar [19].

[edit] 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
Fruit
Apple 13.8 10.4 5.9 2.4 2.1 2.4 19.9
Apricot 11.1 9.2 0.9 2.4 5.9 0.4 63.5
Banana 22.8 12.2 4.9 5.0 2.4 1.0 2.0
Dates 75.0 63.4 19.6 19.9 23.8 1.0 37.6
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 0.8 56.7
Pear 15.5 9.8 6.2 2.8 0.8 2.3 8.0
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 0.9 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 0.7 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 http://www.nal.usda.gov/fnic/foodcomp/search/ [20] All data with a unit of g (gram) are based on 100 g of a food item

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 [21]. There are three types of HFCS, each with a different proportion of fructose. The most common are 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.

[edit] Commercial Sweeteners (% of Carbohydrate)

Sugar Fructose Glucose Sucrose Other Sugars
Granulated Sugar (50) (50) 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. [22] for HFCS, and USDA for fruits and vegetables and the other refined sugars. [23]

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 70’s. Contrary to the popular believe, 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 HFCS, 42 and 55, have relatively 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 [24].

Figure 3 Adjusted U.S. Per Capita Refined Sugar Consumption

[edit] Digestion and Absorption

Fructose exists in foods as either a monosaccharide (free fructose) or as a disaccharide (sucrose). Free fructose does not undergo digestion; 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 and fructose unit. Fructose, passes through the small intestine, virtually unchanged, then enters the portal vein and is directed toward the liver.

Figure 4 The 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. [25] 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

[edit] Capacity and rate of absorption

The absorption capacity for fructose in monosaccharide form ranges from less than 5g to 50g and adapts with changes in dietary fructose intake. Studies show the greatest absorption rate occurs when glucose and fructose are administered in equal quantities [26]. 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 [27]. 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 have been shown to increase abundance of transport proteins within 3 days of intake. [28]

[edit] Malabsorption

Several studies have measured the intestinal absorption of fructose using hydrogen breath test[29] [30] [31] [32] . 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 exchanged across the lungs and measurable by the hydrogen breath test. The colonic flora also produces carbon dioxide, short chain fatty acids, organic acids, and trace gasses in the presence of unabsorbed fructose [33]. The presence of gasses and organic acids in the large intestine causes gastrointestinal symptoms such as bloating, diarrhea, flatulence, and gastrointestial pain [34]. Exercise 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[35].

[edit] Fructose Metabolism

All three dietary monosaccharaides are transported into the liver by the GLUT 2 transporter [36]. 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.

[edit] Fructolysis

Fructolysis can be divided into two main phases: The first phase is the synthesis of the trioses, dihydroxyacetone(DHAP) and glyceraldehyde; the second phase is the subsequent metabolism of these trioses either in the gluconeogenic pathway for glycogen replenishment and/or complete metabolism in the fructolytic pathway to pyruvate, which enters the Krebs cycle, and is converted to citrate and subsequently directed toward ’’de novo’’ synthesis of the free fatty acid palmitate [37].

[edit] The 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.

[edit] 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. It appears that fructose is a better substrate for glycogen synthesis than glucose and that glycogen replenishment takes precedence over triglyceride formation [38]. Once liver glycogen is replenished, the intermediates of fructose metabolism are primarily directed toward triglyceride synthesis.

Figure 6 The Metabolic Conversion of Fructose to Glycogen in the Liver

[edit] 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 [39]. 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 [40]; [41]. Additionally, DHAP can be converted to glycerol 3-phosphate as previously mentioned, providing the glycerol backbone for the triglyceride molecule [42]. 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 The Metabolic Conversion of Fructose to Triglyceride (TG) in the Liver

[edit] Health effects

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Please improve this article if you can (June 2007).

Fructose absorption occurs via the GLUT-5[43] (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.

Excess fructose consumption has been hypothesized to possibly cause insulin resistance, obesity,[44] elevated LDL cholesterol and triglycerides, leading to metabolic syndrome. Short term tests, lack of dietary control, and lack of a non-fructose consuming control group are all confounding factors in human experiments. However, there are now a number of reports showing correlation of fructose consumption to obesity,[45][46] especially central obesity which is generally regarded as the most dangerous type.[citation needed]

There is a concern with Diabetic 1 patients and the apparent low GI of fructose. Fructose gives as high a blood sugar spike as that obtained with glucose. In fact, GI only applies to high starch foods. The basic GI definition is chemically incorrect. This is because the body blood glucose response is "standardized" with 50g of glucose, while the GI Researchers use 50g of digestible carbohydrate as a reference quantity. Although all simple sugars are isomers, each have separate chemical properties. This is illustrated with pure fructose. In a study from The American Journal of Clinical Nutrition, "fructose given alone increased the blood glucose almost as much as a similar amount of glucose (78% of the glucose-alone area)".[47][48][49][49][50]

A study in mice suggests that fructose increases obesity.[51]

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".[52] 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."[53]

Studies that have compared high fructose corn syrup (an ingredient in soft drinks sold in the US) to sucrose (common cane sugar) find that they have essentially identical physiological effects. 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.[54] This is not surprising since sucrose is a disaccharide which digests to 50% glucose and 50% fructose; while the high fructose corn syrup most commonly used on soft drinks is 55% fructose.

Fructose also chelates minerals in the blood. This effect is especially important with micronutrients such as copper, chromium and zinc. Since these solutes are normally present in small quantities, chelation of small numbers of ions may lead to deficiency diseases, immune system impairment and even insulin resistance, a component of type II diabetes.[55]

Fructose is often recommended for diabetics due to its glycemic index being significantly lower than both glucose, sucrose and starches.[citation needed]

"The medical profession thinks fructose is better for diabetics than sugar," says Meira Field, Ph.D., a research chemist associated with the questionable Weston A. Price Foundation [56], "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."[57] This is not entirely true as certain other tissues do use fructose directly, notably the cells of the intestine, and sperm cells (for which fructose is the main energy source).

Fructose is a reducing sugar, as are all monosaccharides. The spontaneous addition of single sugar molecules to proteins, known as glycation, is a significant cause of damage in diabetics. Fructose appears to be as dangerous as glucose in this regard and so does not seem to be a better answer for diabetes for this reason alone.[58] This may be an important contribution to senescence and many age-related chronic diseases.[59]

Fructose is used as a substitute for sucrose (composed of one unit each of fructose and glucose linked together with a relatively weak glycosidic bond) because it is less expensive and has little effect on measured blood glucose levels. Often, fructose is consumed as high fructose corn syrup, which is corn syrup (glucose) that has been enzymatically treated by the enzyme glucose isomerase. This enzyme converts a portion of the glucose into fructose thus making it sweeter. This is done to such a degree as to yield corn syrup with an equivalent sweetness to sucrose by weight. While most carbohydrates have around the same amount of calories, fructose is sweeter and manufacturers can use less of it to get the same result. The free fructose present in fruits, their juice, and honey is responsible for the greater sweetness of these natural sugar sources.

Some studies point to fructose as key factors in hyperactivity and tooth decay in children[citation needed].

Unlike glucose, fructose is almost entirely metabolized in the liver. "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 as compared to glucose results in lower circulating insulin and leptin levels, and attenuation in the suppresion of ghrelin postprandially.[60] These hormones are implicated in the control of appetite and satiety, and it is hypothesized that eating lots of fructose could increase the likelihood of weight gain.[61]

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 sweet drinks is the reason for this.[62]

[edit] See also

[edit] References

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  6. ^ Template:Last=Mirkin
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  8. ^ Oregon State University. "Sugar Sweetness". Last accessed May 5, 2008. http://food.oregonstate.edu/sugar/sweet.html
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  10. ^ "American Sweeteners" (2001): 374-375. 
  11. ^ Hanover, LM; white, JS (1993). "Manufacturing, composition, and application of fructose" 58: 724s-732. 
  12. ^ McWilliams, Margaret (2001). Foods: Experimental Perspectives, 4th Edition. Upper Saddle River, NJ : Prentice Hall. 
  13. ^ "American Sweeteners" (2001): 374-375. 
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  20. ^ Template:Url=http://www.nal.usda.gov/fnic/foodcomp/search/
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v • d • e
Types of Carbohydrates
General:
Geometry
Small/Large
Trioses
Ketotriose (Dihydroxyacetone) | Aldotriose (Glyceraldehyde)
Tetroses
Pentoses
Hexoses
Disaccharides
Polymers
Glycosaminoglycans
Aminoglycosides
Major families of biochemicals
Peptides | Amino acids | Nucleic acids | Carbohydrates | Nucleotide sugars | Lipids | Terpenes | Carotenoids | Tetrapyrroles | Enzyme cofactors | Steroids | Flavonoids | Alkaloids | Polyketides | Glycosides