Difference between revisions of "Fructose" - New World Encyclopedia
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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. | 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; 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 | + | 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. |
==The chemical structure of fructose== | ==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 | + | Fructose is a [[levorotation|levorotatory]] monosaccharide 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, | + | 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. | + | 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 as an energy source== | ||
| − | === | + | ===The absorption of fructose=== |
| − | + | Glucose is absorbed more slowly than glucose and galactose, through a process of [[facilitated diffusion]] (in which transport across biological membranes is assisted by [[transport protein]]s). 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 of mostly 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. | Most dietary fructose is then metabolized by the [[liver]], a control point for the circulation of blood sugar. | ||
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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. | 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. | ||
| − | Fructose may | + | 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]] [[phosphorylate]]s (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: | + | 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, which is preferred by liver: |
| − | # | + | #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 | + | #Glyceraldehyde is then phosphorylated by another enzyme so that it too can enter the glycolytic pathway. |
===Potential health effects of high fructose consumption=== | ===Potential health effects of high fructose consumption=== | ||
| − | Because fructose | + | 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 [[metabolite]]s 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== | ==Disorders involving fructose metabolism== | ||
| − | ''Fructose intolerance'' (''Hereditary Fructose Intolerance'' or ''HFI'') is | + | ''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 [[phosphate]]s 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 | + | ''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'') | + | ''Fructose malabsorption'' (''Dietary Fructose Intolerance'' or ''DFI'') stems from a deficiency of a fructose transporter enzyme in the [[enterocyte]]s (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 a high glucose content help sufferers to absorb fructose. |
| − | == | + | ==High fructose corn syrup== |
===Production=== | ===Production=== | ||
| − | + | [[Image:usda_sweeteners.jpg|thumb|300px|right|United States sweetener consumption, 1966-2004. (Ccane and beet sugar are both pure sucrose.)]] 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 United States over the period 1975–1985, and usage continues to increase (Bray, 2004 & U.S. Department of Agriculture, Economic Research Service, Sugar and Sweetener Yearbook series, Tables 50–52.). | |
| − | |||
| − | |||
| − | |||
| − | + | 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%, 55%, or 90%. The 55% grade is most commonly used in soft drinks and is equivalent to [[caster sugar]]. | |
===The potential impact on human health=== | ===The potential impact on human health=== | ||
| − | + | 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| | |
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). | 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). | ||
| Line 64: | Line 57: | ||
journal=American Journal of Clinical Nutrition|volume=79|issue=4|pages=537-543|month=April|year=2004}}</ref> | 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> | + | 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> [[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== | ||
| Line 73: | Line 65: | ||
*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] | *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] | *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. | + | *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. | *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. | *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. | *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. | *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. | + | *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== | ==External links== | ||
Revision as of 03:55, 21 October 2006
Fructose (or levulose) is a simple sugar (monosaccharide) with the chemical formula (C6H12O6); it is an isomer of glucose. 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, a readily transportable and mobilizable sugar that is stored in the cells of many plants, 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.
Fructose’s Glycemic Index—i.e., 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.
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.
The chemical structure of fructose
Fructose is a levorotatory monosaccharide 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
The absorption of fructose
Glucose 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 of mostly 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
In nearly all organisms, energy from carbohydrates is obtained via glycolysis, a series of biochemical reactions by which one molecule of glucose (Glc) is oxidized to two molecules of pyruvic acid (Pyr), yielding a small net gain of chemical energy. For aerobic organisms such as humans, glycolysis is only the initial stage of carbohydrate 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.
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, which is preferred by liver:
- 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 a high glucose content help sufferers to absorb fructose.
High fructose corn syrup
Production
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 United States over the period 1975–1985, and usage continues to increase (Bray, 2004 & U.S. Department of Agriculture, Economic Research Service, Sugar and Sweetener Yearbook series, Tables 50–52.).
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%, 55%, or 90%. The 55% 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"[1]. A study in mice suggests that fructose increases adiposity.[2] 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, 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.[3]
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. [4] 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."[5]
ReferencesISBN links support NWE through referral fees
- ↑ Bantle, John P. and Susan K. Raatz, William Thomas and Angeliki Georgopoulos (November 2000). Effects of dietary fructose on plasma lipids in healthy subjects. American Journal of Clinical Nutrition 72 (5): 1128-1134.
- ↑ Jurgens, Hella and et al. (2005). Consuming Fructose-sweetened Beverages Increases Body Adiposity in Mice. Obesity Res 13: 1146-1156.
- ↑ Bray, George A. and Samara Joy Nielsen and Barry M. Popkin (April 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.
- ↑ Sugar coated: We're drowning in high fructose corn syrup.
- ↑ Warner, Melanie, "A Sweetener With a Bad Rap", New York Times, 2006-07-02. Retrieved 2006-10-03.
- 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 [1]
- Dennison, Barbara. 1997. Excess Fruit Juice Consumption by Preschool-aged Children Is Associated With Short Stature and Obesity. Pediatrics. 99(1):15-22. [2]
- Havel, P.J. 2005. Dietary fructose: Implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. Nutrition Review. 63(5):133-57. [3]
- 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. 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 [4]
External links
Template:ChemicalSources
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