Difference between revisions of "Fructose" - New World Encyclopedia

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Fructose (or levulose) is a simple sugar (monosaccharide) with the same chemical formula as glucose (C₆H₁₂O₆) but a different atomic arrangement. Along with glucose and galactose, fructose is one of the three most important blood sugars in animals.

Sources of fructose include honey, fruits, and some root vegetables. Fructose is often found in combination with glucose as the disaccharide sucrose (table sugar), a readily transportable and mobilizable sugar that is stored in the cells of many plants, such as sugar beets and sugarcane. In animals, fructose may also be utilized as an energy source, and phosphate derivatives of fructose participate in carbohydrate metabolism.

In addition to natural sources, fructose may be found in commercially produced high fructose corn syrup (HFCS). Like regular corn syrup, HFCS is derived from the hydrolysis of corn starch to yield glucose; however, further enzymatic processing occurs to increase the fructose content. Until recently, fructose has not been present in large amounts in the human diet; thus, the increasing consumption of HFCS as a sweetener in soft drinks and processed foods has been linked to concerns over the rise in obesity and type II diabetes in the United States.

Fructose’s Glycemic Index (an expression of the relative ability of various carbohydrates to raise blood glucose level) is relatively low compared to other simple sugars. Thus, fructose may be recommended for persons with diabetes mellitus or hypoglycemia (low blood sugar), because intake does not trigger high levels of insulin secretion. This benefit is tempered by a concern that fructose may have an adverse effect on plasma lipid and uric acid levels, and that higher blood levels of fructose can be damaging to proteins.

The chemical structure of fructose

The open-chain structure of fructose

Fructose is a levorotatory monosaccharide (counterclockwise rotation of plane polarized light) with the same empirical formula as glucose but with a different structural arrangement of atoms (i.e., it is an isomer of glucose). Like glucose, fructose is a hexose (six-carbon) sugar, but it contains a keto group instead of an aldehyde group, making it a ketohexose.

Like glucose, fructose can also exist in ring form. Its open-chain structure is able to cyclize (form a ring structure) because a ketone can react with an alcohol to form a hemiketal. Specifically, the C-2 keto group of a fructose molecule can react with its C-5 hydroxyl group to form an intramolecular hemiketal. Thus, although fructose is a hexose, it may form a five-membered ring called a furanose, which is the structure that predominates in solution.

Fructose's specific conformation (or structure) is responsible for its unique physical and chemical properties relative to glucose. For example, although the perception of sweetness depends on a variety of factors, such as concentration, pH, temperature, and individual taste buds, fructose is estimated to be approximately 1.2-1.8 times sweeter than glucose.

Fructose as an energy source

Fructose absorption

Fructose is absorbed more slowly than glucose and galactose, through a process of facilitated diffusion (in which transport across biological membranes is assisted by transport proteins). Large amounts of fructose may overload the absorption capacity of the small intestine, resulting in diarrhea. For example, young children who drink a lot of fruit juice that is composed mainly of fructose may suffer from “toddlers’ diarrhea.” Fructose is absorbed more successfully when ingested with glucose, either separately or as sucrose.

Most dietary fructose is then metabolized by the liver, a control point for the circulation of blood sugar.

The breakdown of fructose

Energy from carbohydrates is obtained by nearly all organisms via glycolysis. It is only the initial stage of carbohydrate catabolism for aerobic organisms such as humans. The end-products of glycolysis typically enter into the citric acid cycle and the electron transport chain for further oxidation, producing considerably more energy per glucose molecule.

Fructose may enter the glycolytic pathway by two major routes: one predominant in liver, the other in adipose tissue (a specialized fat-storage tissue) and skeletal muscle. In the latter, the degradation of fructose closely resembles the catabolism of glucose: the enzyme hexokinase phosphorylates (adds a phosphate) to form fructose-6-phosphate, an intermediate of glycolysis.

The liver, in contrast, handles glucose and fructose differently. There are three steps involved in the fructose-1-phosphate pathway, which is preferred by liver due to its high concentration of fructokinase relative to hexokinase:

Fructose is phosphorylated by the enzyme fructokinase to fructose-1-phosphate.
The six-carbon fructose is split into two three-carbon molecules, glyceraldehyde and dihydroxyacetone phosphate.
Glyceraldehyde is then phosphorylated by another enzyme so that it too can enter the glycolytic pathway.

Potential health effects of high fructose consumption

Because the liver metabolizes fructose differently than glucose, its breakdown also has different biochemical and physiological effects. Fructose metabolism provides the liver with an abundance of pyruvate and lactate for further degradation, so that metabolites of the citric acid cycle, such as citrate and malate, also build up. Citrate can be converted to acetyl CoA, which serves as a precursor for fatty acid synthesis or cholesterol synthesis. Thus, a long-term increase in fructose or sucrose consumption can lead to increased plasma levels of triglyceride and lactate, as well as increased lipid storage in adipose tissue.

Disorders involving fructose metabolism

Fructose intolerance (Hereditary Fructose Intolerance or HFI) is caused by an inherited deficiency of the enzyme Fructose-1-phosphate aldolase-B. The absence of this enzyme prevents the breakdown of fructose beyond its intermediate fructose-1-phosphate. The resulting accumulation of fructose-1-phosphate and depletion of phosphates for ATP production in the liver blocks both the synthesis of glucose (gluconeogenesis) and the release of glucose through the breakdown of glycogen (glycogenolysis). If fructose is ingested, vomiting and hypoglycemia will result; long-term effects include a decline in liver function and possible kidney failure.

Fructosuria, in contrast, is caused by a genetic defect in the enzyme fructokinase. This benign disorder results in the excretion of fructose in the urine.

Fructose malabsorption (Dietary Fructose Intolerance or DFI) stems from a deficiency of a fructose transporter enzyme in the enterocytes (specialized cells found on the surface of the intestines). In fructose malabsorption, the small intestine fails to absorb fructose properly. In the large intestine, the unabsorbed fructose is metabolized by normal colonic bacteria to short-chain fatty acids and the gases hydrogen, carbon dioxide, and methane, which leads to symptoms of abdominal bloating, diarrhea, or constipation. Foods with high glucose content help sufferers to absorb fructose.

High fructose corn syrup

Production

The production process of high fructose corn syrup (HFCS) was developed by Japanese researchers in the 1970s. HFCS was rapidly introduced in many processed foods and soft drinks in the United States over the period 1975–1985, and usage continues to increase (Bray et al. 2004).

The preference for fructose over glucose or sucrose in U.S. commercial food production can be explained in part by its cheaper cost, due to corn subsidies and import sugar tariffs. In addition, fructose does not form crystals at acid pH and has better freezing properties than sucrose, which leads to easier transport and a longer shelf life for food products.

Common commercial grades of high fructose corn syrup include fructose contents of 42 percent, 55 percent, or 90 percent. The 55 percent grade is most commonly used in soft drinks and is equivalent to caster sugar.

The potential impact on human health

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" (Bantle et al. 2000). A study in mice suggests that fructose increases adiposity (amount of body fat or adipose tissue) (Jurgens et al. 2005). However, these studies looked at the effects of fructose alone. As noted by the U.S. Food and Drug Administration (FDA) in 1996, the saccharide composition (glucose to fructose ratio) of HFCS is approximately the same as that of honey, invert sugar, and the disaccharide sucrose.

A more recent study found a link exists between obesity and high HFCS consumption, especially from soft drinks (Bray et al. 2004). While the over-consumption of HFCS may be a contributor to the epidemic of obesity and Type II diabetes in the United States, the obesity epidemic has many contributing factors. University of California, Davis nutrition researcher Peter Havel has pointed out that while there are likely differences between sweeteners, "the increased consumption of fat, the increased consumption of all sugars, and inactivity are all to blame for the obesity epidemic" (Warner 2006).

References
ISBN links support NWE through referral fees

Bantle, J., S. K. Raatz, W. Thomas, and A. Georgopoulos. 2000. “Effects of dietary fructose on plasma lipids in healthy subjects.” American Journal of Clinical Nutrition 72 (5): 1128-1134.
Barasi, M. E. 2003. Human Nutrition: A Health Perspective. London: Hodder Arnold. ISBN 978-0340810255
Bray, G. A., S. J. Nielsen, and B. M. Popkin. 2004. “Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity.” American Journal of Clinical Nutrition 79 (4): 537-543.
Dennison, B. 1997. “Excess fruit juice consumption by preschool-aged children is associated with short stature and obesity.” Pediatrics 99 (1): 15-22.
Havel, P. J. 2005. “Dietary fructose: Implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism.” Nutrition Review 63 (5): 133-157.
Jurgens, H. et al. 2005. “Consuming fructose-sweetened beverages increases body adiposity in mice.” Obesity Research 13: 1146-1156.
Levi, B., and M. J. Werman. 1998. “Long-term fructose consumption accelerates glycation and several age-related variables in male rats.” Journal of Nutrition 128: 1442-1449.
Mann, J., and Stewart Truswell (eds.). 2012. Essentials of Human Nutrition. Oxford: Oxford University Press. ISBN 978-0199566341
McPherson, J. D, B. H. Shilton, and D. J. Walton. 1988. “Role of fructose in glycation and cross-linking of proteins.” Biochemistry 27: 1901-1907.
Stryer, L. 1995. Biochemistry. New York: W.H. Freeman. ISBN 978-0716720096
Stipanuk, M. H. 2006. Biochemical, Physiological, and Molecular Aspects of Human Nutrition. St. Louis, MO: Saunders/Elsevier. ISBN 978-1416002093
Warner, M. 2006. “A sweetener with a bad rap.” New York Times July 2, 2006.
Wylie-Rosett, J. et al. 2004. “Carbohydrates and increases in obesity: Does the type of carbohydrate make a difference?” Obesity Research 12: 124S-129S.

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@@ Line 1: / Line 1: @@
-{{Contracted}}
+{{Copyedited}}{{Paid}}{{Approved}}{{Images OK}}{{Submitted}}
-'''Fructose''' (or '''levulose''') is a simple [[sugar]] ([[monosaccharide]]) with the chemical formula ([[carbon|C]]<sub>6</sub>[[hydrogen|H]]<sub>12</sub>[[oxygen|O]]<sub>6</sub>); it is an [[isomer]] of [[glucose]]. Along with glucose and [[galactose]], fructose is one of the three most important [[blood sugar]]s in [[animal]]s.
+'''Fructose''' (or '''levulose''') is a simple [[sugar]] ([[Carbohydrate#Monosaccharides|monosaccharide]]) with the same chemical formula as [[glucose]] ([[carbon|C]]<sub>6</sub>[[hydrogen|H]]<sub>12</sub>[[oxygen|O]]<sub>6</sub>) but a different atomic arrangement. Along with glucose and [[galactose]], fructose is one of the three most important [[blood]] sugars in [[animal]]s.
-Sources of fructose include [[honey]], [[fruit]]s, and some root [[vegetable]]s. Fructose is often found in combination with glucose as the disaccharide [[sucrose]], a readily transportable and mobilizable sugar that is stored in the [[cell]]s of many [[plant]]s, such as sugar beets and sugar cane. In animals, fructose may also be utilized as an energy source, and [[phosphate]] derivatives of fructose participate in [[carbohydrate]] metabolism.
+Sources of fructose include [[honey]], [[fruit]]s, and some root [[vegetable]]s. Fructose is often found in combination with glucose as the disaccharide [[sucrose]] (table sugar), a readily transportable and mobilizable sugar that is stored in the [[cell (biology)|cell]]s of many [[plant]]s, such as [[sugar beet]]s and [[sugarcane]]. In animals, fructose may also be utilized as an energy source, and phosphate derivatives of fructose participate in [[carbohydrate]] metabolism.
-Fructose’s [[Glycemic Index]]—i.e., an expression of the relative ability of various [[carbohydrate]]s to raise blood glucose level—is relatively low compared to other simple sugars. Thus, fructose may be recommended for persons with [[diabetes mellitus]] or [[hypoglycemia]] (low blood sugar), because intake does not trigger high levels of [[insulin]] secretion. This benefit is tempered by a concern that fructose may have an adverse effect on plasma [[lipid]] and uric acid levels and that higher blood levels of fructose can be damaging to [[protein]]s.
+In addition to natural sources, fructose may be found in commercially produced ''high fructose corn syrup'' (HFCS). Like regular [[corn]] syrup, HFCS is derived from the hydrolysis of corn [[starch]] to yield glucose; however, further enzymatic processing occurs to increase the fructose content. Until recently, fructose has not been present in large amounts in the human diet; thus, the increasing consumption of HFCS as a sweetener in soft drinks and processed foods has been linked to concerns over the rise in obesity and type II [[diabetes]] in the United States.
+{{toc}}
-In addition to natural sources, fructose may be found in commercially produced [[high fructose corn syrup]] (HFCS) Like regular [[corn syrup]], HFCS is derived from the hydrolysis of [[corn starch]] to yield glucose; in HFCS, however, further enzymatic processing occurs to increase the fructose content. Given that traditionally fructose was not present in large amounts in the human diet, the increasing consumption of HFCS as a sweetener in soft drinks and processed foods has been linked to concerns over the rise in obesity and type II diabetes in the United States. However, these health trends have multiple contributing factors.
+Fructose’s ''Glycemic Index'' (an expression of the relative ability of various carbohydrates to raise blood glucose level) is relatively low compared to other simple sugars. Thus, fructose may be recommended for persons with [[diabetes mellitus]] or [[hypoglycemia]] (low blood sugar), because intake does not trigger high levels of [[insulin]] secretion. This benefit is tempered by a concern that fructose may have an adverse effect on plasma [[lipid]] and uric acid levels, and that higher blood levels of fructose can be damaging to [[protein]]s.
 ==The chemical structure of fructose==
-[[Image:D-fructose.png|120px|right|thumb|The open-chain structure of fructose.]]
+[[Image:D-fructose.png|120px|right|thumb|The open-chain structure of fructose]]
-Fructose is a [[levorotation|levorotatory]] monosaccharide with the same empirical formula as [[glucose]] but with a different structure (i.e., it is an isomer of glucose). Like glucose, fructose is a ''hexose'' (six-carbon) sugar, but it contains a [[keto]] group instead of an [[aldehyde]] group, making it a ''ketohexose''.
+Fructose is a levorotatory monosaccharide (counterclockwise rotation of plane polarized light) with the same empirical formula as [[glucose]] but with a different structural arrangement of atoms (i.e., it is an isomer of glucose). Like glucose, fructose is a ''hexose'' (six-carbon) sugar, but it contains a keto group instead of an aldehyde group, making it a ''ketohexose''.
-Like glucose, the fructose can also exist in ring form. Its open-chain structure is able to cyclize (form a ring) because a ketone can react with an alcohol to form a [[hemiketal]]. Specifically, the C-2 keto group in the open-chain form of fructose can react with its C-5 hydroxyl group to form an ''intramolecular hemiketal''. Thus, although fructose is a hexose, it may forms a five-membered ring called a [[furanose]], a structure that predominates in solution.
+Like glucose, fructose can also exist in ring form. Its open-chain structure is able to cyclize (form a ring structure) because a ketone can react with an alcohol to form a hemiketal. Specifically, the C-2 keto group of a fructose molecule can react with its C-5 hydroxyl group to form an ''intramolecular hemiketal''. Thus, although fructose is a hexose, it may form a five-membered ring called a ''furanose'', which is the structure that predominates in solution.
-Fructose's specific [[conformation]] (or structure) is responsible for its unique physical and chemical properties relative to glucose. Although the perception of sweetness depends on a variety of factors, such as concentration, pH, temperature, and individual taste buds, fructose is estimated to be approximately 1.2-1.8 times sweeter than glucose.
+Fructose's specific conformation (or structure) is responsible for its unique physical and chemical properties relative to glucose. For example, although the perception of sweetness depends on a variety of factors, such as concentration, pH, temperature, and individual taste buds, fructose is estimated to be approximately 1.2-1.8 times sweeter than glucose.
 == Fructose as an energy source==
-===Digestion and absorption===
+===Fructose absorption===
-Dietary fructose is absorbed more slowly than glucose and galactose, through a process of [[facilitated diffusion]]. Large amounts at any one time may overload the absorption capacity of the small intestine, resulting in diarrhea. For example, young children who drink a lot of juice whose sugar is mostly fructose may suffer from “toddlers’ diarrhea.” Fructose is absorbed better when ingested with glucose, either separately or as sucrose.
+Fructose is absorbed more slowly than glucose and galactose, through a process of facilitated diffusion (in which transport across biological membranes is assisted by transport proteins). Large amounts of fructose may overload the absorption capacity of the small intestine, resulting in [[diarrhea]]. For example, young children who drink a lot of fruit juice that is composed mainly of fructose may suffer from “toddlers’ diarrhea.” Fructose is absorbed more successfully when ingested with [[glucose]], either separately or as [[sucrose]].
 Most dietary fructose is then metabolized by the [[liver]], a control point for the circulation of blood sugar.
-===Metabolism===
+===The breakdown of fructose===
-In nearly all organisms, energy from [[carbohydrates]] is obtained via [[glycolysis]], a series of [[biochemistry|biochemical]] reactions by which one [[molecule]] of [[Glucose|glucose (Glc)]] is [[oxidized]] to two molecules of pyruvic acid (Pyr), yielding a small net gain of chemical energy. For aerobic organisms such as [[human]]s, glycolysis is only the initial stage of [[carbohydrate]] [[metabolism|catabolism]]; the end-products of glycolysis  typically enter into the [[citric acid cycle]] (also known as the TCA or Krebs cycle) and the electron transport chain for further oxidation. These pathways together produce considerably more energy per glucose molecule than anaerobic oxidation.
+Energy from [[carbohydrate]]s is obtained by nearly all organisms via [[glycolysis]]. It is only the initial stage of carbohydrate [[metabolism|catabolism]] for aerobic organisms such as humans. The end-products of glycolysis typically enter into the [[citric acid cycle]] and the electron transport chain for further oxidation, producing considerably more energy per glucose molecule.
-Fructose may be metabolized by two major pathways, one predominant in liver; the other in adipose tissue (a specialized [[fat]]-storage tissue) and skeletal muscle. In the latter organs, the degradation of fructose closely resembles the catabolism of glucose: fructose is phosphorylated (a phosphate is added) to fructose-6-phosphate, an [[intermediate]] of glycolysis, by the enzyme [[hexokinase]].
+Fructose may enter the glycolytic pathway by two major routes: one predominant in liver, the other in adipose tissue (a specialized [[fat]]-storage tissue) and skeletal [[muscle]]. In the latter, the degradation of fructose closely resembles the catabolism of glucose: the enzyme hexokinase phosphorylates (adds a phosphate) to form ''fructose-6-phosphate'', an intermediate of glycolysis.
-In liver, fructose must undergo a few modifications before it is able to enter the glycolytic pathway. There are three steps involved in the fructose-1-phosphate pathway, preferred by liver:
+The [[liver]], in contrast, handles glucose and fructose differently. There are three steps involved in the fructose-1-phosphate pathway, which is preferred by liver due to its high concentration of fructokinase relative to hexokinase:
-#The [[phosphorylation]] of fructose by the enzyme [[fructokinase]] to fructose-1-phosphate.
+#Fructose is phosphorylated by the enzyme fructokinase to ''fructose-1-phosphate''.
-#A split of the six-carbon fructose into two three-carbon molecules, ‘’glyceraldehyde’’ and ‘’dihydroxyacetone phosphate’’ (an aldol cleavage).
+#The six-carbon fructose is split into two three-carbon molecules, ''glyceraldehyde'' and ''dihydroxyacetone phosphate''.
-#Glyceraldehyde is then phosphorylated by another enzyme so that it too can enter glycolysis.
+#Glyceraldehyde is then phosphorylated by another enzyme so that it too can enter the glycolytic pathway.
 ===Potential health effects of high fructose consumption===
-Because fructose is metabolized in a different way in liver, its breakdown has different biochemical and physiological effects than the degradation of glucose. Fructose breakdown provides the liver with an abundance of pyruvate and lactate for further degradation, so that metabolites of the citric acid cycle, such as citrate and malate, also build up. Citrate can be converted to acetyl CoA, which serves as a precursor for fatty acid synthesis or cholesterol synthesis. Overall, a long-term increase in fructose or sucrose consumption can lead to increased plasma levels of [[triglyceride]] and lactate, as well as increased lipid storage in adipose tissue.
+Because the liver metabolizes fructose differently than glucose, its breakdown also has different biochemical and physiological effects. Fructose metabolism provides the liver with an abundance of pyruvate and lactate for further degradation, so that metabolites of the [[citric acid cycle]], such as citrate and malate, also build up. Citrate can be converted to acetyl CoA, which serves as a precursor for [[fatty acid]] synthesis or [[cholesterol]] synthesis. Thus, a long-term increase in fructose or sucrose consumption can lead to increased plasma levels of triglyceride and lactate, as well as increased lipid storage in adipose tissue.
-Glycemic load (GL) a more useful concept, as it takes into consideration the amount of carb consumed (170) research suggests link to risk of type 2 diab, heart disease, and obesity
+==Disorders involving fructose metabolism==
+''Fructose intolerance'' (''Hereditary Fructose Intolerance'' or ''HFI'') is caused by an inherited deficiency of the [[enzyme]] ''Fructose-1-phosphate aldolase-B''. The absence of this enzyme prevents the breakdown of fructose beyond its intermediate ''fructose-1-phosphate''. The resulting accumulation of fructose-1-phosphate and depletion of phosphates for [[ATP]] production in the liver blocks both the synthesis of glucose ([[gluconeogenesis]]) and the release of glucose through the breakdown of [[glycogen]] (glycogenolysis). If fructose is ingested, vomiting and hypoglycemia will result; long-term effects include a decline in [[liver]] function and possible [[kidney]] failure.
-==Disorders involving fructose metabolism==
+''Fructosuria'', in contrast, is caused by a genetic defect in the enzyme fructokinase. This benign disorder results in the excretion of fructose in the urine.
-''Fructose intolerance'' (''Hereditary Fructose Intolerance'' or ''HFI'') is a [[hereditary condition]] involving the deficiency of an enzyme called ''Fructose-1-phosphate aldolase-B''. The absence of this enzyme prevents the metabolism of fructose beyond fructose-1-phosphate. The resulting accumulation of fructose-1-phosphate and depletion of [[phosphate]]s for ATP production in the liver blocks the synthesis of glucose ([[gluconeogenesis]]) as well as the release of glucose through the breakdown of [[glycogen]] ([[glycogenolysis]]). If fructose is ingested, vomiting and severe hypoglycemia will result, and long-term effects include a decline in liver function and possible kidney failure.
-''Fructosuria'', in contrast, is caused by a genetic defect in the enzyme fructokinase. This relatively mild disorder results in the excretion of fructose in the urine.
+''Fructose malabsorption'' (''Dietary Fructose Intolerance'' or ''DFI'') stems from a deficiency of a fructose transporter enzyme in the enterocytes (specialized cells found on the surface of the intestines). In fructose malabsorption, the small intestine fails to absorb fructose properly. In the large intestine, the unabsorbed fructose is metabolized by normal colonic bacteria to short-chain [[fatty acid]]s and the gases hydrogen, carbon dioxide, and methane, which leads to symptoms of abdominal bloating, diarrhea, or constipation. Foods with high glucose content help sufferers to absorb fructose.
-''Fructose malabsorption'' (''Dietary Fructose Intolerance'' or ''DFI'') is a deficiency of a fructose transporter enzyme in the [[enterocyte]]s, which leads to abdominal [[bloating]], [[diarrhea]] and/or [[constipation]]. In patients with fructose malabsorption, the small intestine fails to absorb fructose properly. In the large intestine, the unabsorbed fructose osmotically reduces the absorption of water and is metabolized by normal colonic bacteria to short chain fatty acids and the gases hydrogen, carbon dioxide and methane. Foods with a high glucose content help sufferers absorb fructose.
+==High fructose corn syrup==
-==The commercial use of high fructose corn syrup==
 ===Production===
-'''High fructose corn syrup''' (HFCS) is a newer and sweeter form of [[corn syrup]]. Like ordinary [[corn syrup]], the high fructose variety is made from [[corn starch]] using enzymes. The production process of HFCS was developed by Japanese researchers in the [[1970s]]. HFCS was rapidly introduced in many processed foods and soda drinks in the US over the period of about 1975–1985, and usage continues to increase as sugar use decreases at a nearly one to one level (Bray, 2004 & U.S. Department of Agriculture, Economic Research Service, Sugar and Sweetener Yearbook series, Tables 50–52.).
-There are three main reasons for this switch; first is cost, as HFCS is a bit cheaper due to corn subsidies and import sugar tariffs. The second reason is that it is a liquid which is easier to blend and transport.  The third is that a product made with HFCS has a much longer shelf life. (White JS. 1992. Fructose syrup: production, properties and applications, in FW Schenck & RE Hebeda, eds, Starch Hydrolysis Products – Worldwide Technology, Production, and Applications. VCH Publishers, Inc. 177-200)
-By increasing the [[fructose]] content of corn syrup ([[glucose]]) through enzymatic processing, the syrup is more comparable to table sugar ([[sucrose]]). This makes it useful to manufacturers as a possible substitute for sugar in soft drinks and other processed foods. Common commercial grades of high fructose corn syrup include fructose contents of 42%, 55%, or 90%. The 55% grade is most commonly used in soft drinks and is equivalent to [[caster sugar]].
+The production process of high fructose corn syrup (HFCS) was developed by Japanese researchers in the 1970s. HFCS was rapidly introduced in many processed foods and soft drinks in the United States over the period 1975–1985, and usage continues to increase (Bray et al. 2004).
-===Sweetener consumption patterns===
+The preference for fructose over [[glucose]] or [[sucrose]] in U.S. commercial food production can be explained in part by its cheaper cost, due to [[corn]] subsidies and import sugar tariffs. In addition, fructose does not form crystals at acid pH and has better freezing properties than sucrose, which leads to easier transport and a longer shelf life for food products.
-[[Image:usda_sweeteners.jpg|thumb|300px|right|US sweetener consumption, 1966-2004 (cane and beet sugar are both pure [[sucrose]])]]
-The accompanying graph shows the consumption of sweeteners per capita in the United States since 1966. Since HFCS and sucrose (cane and beet sugars) provide almost identical proportions of fructose and glucose, no metabolic changes would be expected from substituting one for the other. However, it is apparent from this graph that overall sweetener consumption, and in particular glucose-fructose mixtures, has increased since the introduction of HFCS. Thus, the proportion of fructose as a component of overall sweetener intake in the United States has increased since the early 1980s. This would be true whether the added sweetener was HFCS, table sugar, or any other glucose-fructose mixture.
-HFCS is produced in the industrialized countries. The production of HFCS is dependent on the agricultural, especially sugar, policy. In [[Europe]], due to the fact that HFCS (isoglucose) is under the adjustment of production, the greater availability of [[cane sugar]] over [[maize]] would make its production there uneconomical. In Japan, HFCS consumption accounts for one quarter of total sweetener consumption.
+Common commercial grades of high fructose corn syrup include fructose contents of 42 percent, 55 percent, or 90 percent. The 55 percent grade is most commonly used in soft drinks and is equivalent to caster [[sugar]].
 ===The potential impact on human health===
-While most [[carbohydrates]] have around the same amount of [[calories]], fructose is generally perceived as sweeter than glucose, so [[manufacturers]] may use less fructose to achieve the same perception of sweetness as found in sucrose. One study concluded that fructose "produced significantly higher fasting plasma [[Triglyceride|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"<ref>{{Cite journal|last=Bantle|first=John P.|coauthors=Susan K. Raatz, William Thomas and Angeliki Georgopoulos|url=http://www.ajcn.org/cgi/content/full/72/5/1128|title=Effects of dietary fructose on plasma lipids in healthy subjects|
+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" (Bantle et al. 2000). A study in mice suggests that fructose increases adiposity (amount of body fat or adipose tissue) (Jurgens et al. 2005). However, these studies looked at the effects of fructose alone. As noted by the U.S. Food and Drug Administration (FDA) in 1996, the saccharide composition (glucose to fructose ratio) of HFCS is approximately the same as that of honey, invert sugar, and the disaccharide [[sucrose]].
-journal=American Journal of Clinical Nutrition|volume=72|issue=5|pages=1128-1134|month=November|year=2000 }}</ref>. A study in mice suggests that fructose increases [[adiposity]].<ref>{{Cite journal|last=Jurgens|first=Hella|coauthors=et al.|url=http://www.obesityresearch.org/cgi/content/abstract/13/7/1146|title=Consuming Fructose-sweetened Beverages Increases Body Adiposity in Mice|journal=Obesity Res|volume=13|pages=1146-1156|year=2005}}</ref> However, these studies looked at the effects of fructose alone. As noted by the U.S. [[Food and Drug Administration]] in 1996, the saccharide composition (glucose to fructose ratio) of HFCS is approximately the same as that of honey, [[Inverted sugar syrup|invert sugar]] and the disaccharide sucrose (or table sugar).
-A more recent study found a link exists between [[obesity]] and high HFCS consumption, especially from soft drinks.<ref>{{Cite journal|last=Bray|first=George A.|coauthors=Samara Joy Nielsen and Barry M. Popkin|url=http://www.ajcn.org/cgi/content/full/79/4/537|title=Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity|
-journal=American Journal of Clinical Nutrition|volume=79|issue=4|pages=537-543|month=April|year=2004}}</ref>
-While the over-consumption of HFCS may be a contributor to the epidemic of obesity and Type II diabetes in the United States, the obesity epidemic has many contributing factors. <ref>[http://www.sfgate.com/cgi-bin/article.cgi?f=/chronicle/archive/2004/02/18/FDGS24VKMH1.DTL Sugar coated:  We're drowning in high fructose corn syrup.]</ref>
+A more recent study found a link exists between [[obesity]] and high HFCS consumption, especially from soft drinks (Bray et al. 2004). While the over-consumption of HFCS may be a contributor to the epidemic of obesity and Type II diabetes in the United States, the obesity epidemic has many contributing factors. University of California, Davis nutrition researcher Peter Havel has pointed out that while there are likely differences between sweeteners, "the increased consumption of [[fat]], the increased consumption of all [[sugar]]s, and inactivity are all to blame for the obesity epidemic" (Warner 2006).
-However, the obesity epidemic has many contributing factors. [[University of California, Davis]] nutrition researcher Peter Havel has pointed out that while there are likely differences between sweeteners, "the increased consumption of fat, the increased consumption of all sugars, and inactivity are all to blame for the obesity epidemic."<ref>{{Cite news|first=Melanie|last=Warner|title=A Sweetener With a Bad Rap|url=http://www.nytimes.com/2006/07/02/business/yourmoney/02syrup.html?pagewanted=all|publisher=New York Times|date=2006-07-02|accessdate=2006-10-03}}</ref>
 ==References==
-<references />
-*Barasi, Mary E. 2003. ''Human Nutrition: A Health Perspective'', 2nd edition. London: Arnold.
-*Bray, George A. 2004. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. ''American Journal of Clinical Nutrition''. 79(4):537-543. April 2004 [http://www.ajcn.org/cgi/content/full/79/4/537]
-*Dennison, Barbara. 1997. Excess Fruit Juice Consumption by Preschool-aged Children Is Associated With Short Stature and Obesity. ''Pediatrics''. 99(1):15-22. [http://pediatrics.aappublications.org/cgi/content/full/99/1/15]
-*Havel, P.J. 2005. Dietary fructose: Implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. ''Nutrition Review.'' 63(5):133-57. [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11743131&itool=iconfft&query_hl=20]
-*Levi B. and M.J. Werman. 1998. Long-term fructose consumption accelerates glycation and several age-related variables in male rats. "Journal of Nutrition''. 128:1442-9. [http://www.nutrition.org/cgi/content/full/128/9/1442 Fulltext]. PMID 9732303.
-*Mann, Jim and A. Stewart Truswell, eds. 2002. ''Essentials of Human Nutrition'', 2nd edition. Oxford: Oxford University Press.
-*McPherson, J.D, B.H. Shilton, and D.J. Walton. 1988. Role of fructose in glycation and cross-linking of proteins. ''Biochemistry''. 27:1901-7.
-*Stryer, Lubert. 1995. ''Biochemistry'', 4th edition. New York, NY: W.H. Freeman.
-*Stipanuk, Martha H. 2006. ''Biochemical, Physiological, and Molecular Aspects of Human Nutrition'', 2nd edition. St. Louis, MO: Saunders/Elsevier.
-*Wylie-Rosett, Judith, et al. 2004.'Carbohydrates and Increases in Obesity: Does the Type of Carbohydrate Make a Difference? ''Obesity Research''. 12:124S-129S [http://www.obesityresearch.org/cgi/content/full/12/suppl_2/124S]
-==External links==
-{{ChemicalSources}}
-{{credit|71493629}}
+* Bantle, J., S. K. Raatz, W. Thomas, and A. Georgopoulos. 2000. “Effects of dietary fructose on plasma lipids in healthy subjects.” ''American Journal of Clinical Nutrition'' 72 (5): 1128-1134.
+* Barasi, M. E. 2003. ''Human Nutrition: A Health Perspective''. London: Hodder Arnold. ISBN 978-0340810255
+* Bray, G. A., S. J. Nielsen, and B. M. Popkin. 2004. “Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity.” ''American Journal of Clinical Nutrition'' 79 (4): 537-543.
+* Dennison, B. 1997. “Excess fruit juice consumption by preschool-aged children is associated with short stature and obesity.” ''Pediatrics'' 99 (1): 15-22.
+* Havel, P. J. 2005. “Dietary fructose: Implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism.” ''Nutrition Review'' 63 (5): 133-157.
+* Jurgens, H. et al. 2005. “Consuming fructose-sweetened beverages increases body adiposity in mice.” ''Obesity Research'' 13: 1146-1156.
+* Levi, B., and M. J. Werman. 1998. “Long-term fructose consumption accelerates glycation and several age-related variables in male rats.” ''Journal of Nutrition'' 128: 1442-1449.
+* Mann, J., and Stewart Truswell (eds.). 2012. ''Essentials of Human Nutrition''. Oxford: Oxford University Press. ISBN 978-0199566341
+* McPherson, J. D, B. H. Shilton, and D. J. Walton. 1988. “Role of fructose in glycation and cross-linking of proteins.” ''Biochemistry'' 27: 1901-1907.
+* Stryer, L. 1995. ''Biochemistry''. New York: W.H. Freeman. ISBN 978-0716720096
+* Stipanuk, M. H. 2006. ''Biochemical, Physiological, and Molecular Aspects of Human Nutrition''. St. Louis, MO: Saunders/Elsevier. ISBN 978-1416002093
+* Warner, M. 2006. “A sweetener with a bad rap.” ''New York Times'' July 2, 2006.
+* Wylie-Rosett, J. et al. 2004. “Carbohydrates and increases in obesity: Does the type of carbohydrate make a difference?” ''Obesity Research'' 12: 124S-129S.
+{{credits|Fructose|71493629|Fructose_intolerance|81319314|Fructose_malabsorption|84456352|High_fructose_corn_syrup|84520642}}
 [[Category:Life sciences]]
+[[Category:Biochemistry]]
+[[Category:Food]]