Difference between revisions of "Fructose" - New World Encyclopedia

From New World Encyclopedia
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'''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]] ([[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.  
  
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 many plant cells, such as in sugar beets and sugar cane. In animals, fructose may also be utilized as an energy source, and [[phosphate]] derivatives of fructose participate in the metabolism of [[carbohydrates]].
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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.
  
Fructose’s [[Glycemic Index]]—i.e., the measure of the speed at which particular carbohydrates are converted into glucose in the body—is relatively low compared to other simple sugars because of its slower absorption into the bloodstream. Thus, fructose may be recommended for patients 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.  
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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.  
  
In addition to natural sources, fructose may be found in commercially produced [[high fructose corn syrup]] (HFCS), in which the fructose content of corn syrup ([[glucose]]) is increased through enzymatic processing. 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 (“table sugar”). This property makes HFCS useful to manufacturers as a possible substitute for sugar in soft drinks and other processed foods. There are currently suspicions that over-consumption of HFCS may be a contributor to the epidemic of obesity and Type II diabetes in the United States. However, 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>
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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.
  
 
==The chemical structure of fructose==
 
==The chemical structure of fructose==
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== Fructose as an energy source==
 
== Fructose as an energy source==
Most of the dietary fructose passes through the [[liver]], a control point for the circulation of blood sugar.
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===Digestion and absorption===
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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.
  
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Most dietary fructose is then metabolized by the [[liver]], a control point for the circulation of blood sugar.
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===Metabolism===
 
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.
  
Unlike glucose, fructose must undergo a few modifications before it is able to enter the glycolytic pathway. One method occurs in the fructose-1-phosphate pathway, preferred by the liver. There are three steps involved:
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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]].
#The [[phosphorylation]] (addition of a phosphate molecule) of fructose by the enzyme [[fructokinase]].  
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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 [[phosphorylation]] of fructose 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).  
 
#A split of the six-carbon fructose into two three-carbon molecules, ‘’glyceraldehyde’’ and ‘’dihydroxyacetone phosphate’’ (an aldol cleavage).  
 
#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 glycolysis.
  
Alternatively, fructose can enter via another route: it can be phosphorylated to fructose-6-phosphate (F6P) by the enzyme [[hexokinase]]. Little F6P is formed in the liver given the abundance of glucose relative to fructose. In contrast, [[adipose]] tissue (a specialized [[fat]]-storage tissue) has much more fructose than glucose. Thus, most of the fructose in adipose tissue is mobilized by this latter pathway.
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===Potential health effects of high fructose consumption===
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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.
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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==
 
==Disorders involving fructose metabolism==
'''Fructose intolerance''('''Hereditary Fructose Intolerance''', or '''HFI''') is a [[hereditary condition]] —a deficiency of liver [[enzyme]]s that metabolize [[fructose]]. The deficient enzyme is [[Fructose-1-phosphate aldolase-B]], this means that the fructose cannot be further metabolised beyond fructose-1-phosphate. This traps [[phosphate]]s; which are needed to phosphorolyse [[glycogen phosphorolase]] to carry on to make [[glucose]]. Therefore glucose cannot be made through the breakdown of [[glycogen]] nor from [[gluconeogenesis]], resulting in severe [[hypoglycaemia]]. If fructose is ingested, vomiting, hypoglycaemia and eventually kidney failure will follow.
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''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.
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''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.
  
Hereditary Fructose Intolerance should not be confused with [[fructose malabsorption]] or Dietary Fructose Intolerance (DFI), a deficiency of fructose transporter enzyme in the [[enterocytes]], 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 actually help sufferers absorb fructose.  
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''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.
  
 
==The commercial use of high fructose corn syrup==
 
==The commercial use of high fructose corn syrup==
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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)
 
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 equivalent to [[caster sugar]].
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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]].
  
 
===Sweetener consumption patterns===
 
===Sweetener consumption patterns===
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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.
 
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.
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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.
 
 
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.
 
  
 
===The potential impact on human health===
 
===The potential impact on human health===
The average American consumed approximately 19.2 kg of HFCS versus 20 kg of sugar in 2004.{{fact}}<!-- The graph on the right shows consumption of each as being nearer 60lb, consistent with the WHO figures —> Where HFCS is not used or rarely used, the sugar consumption per person can be higher than the USA; for example, the 2002 figures for some countries are: USA 32.4 kg, EU 40.1 kg, Brazil 59.7 kg, and Australia 56.2 kg.<ref>WHO Oral Health Country/Area Profile Programme [http://www.example.com Global Sugar Consumption]</ref>
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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 [[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).
  
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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>
  
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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>
 
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>
 
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==
 
<references />
 
<references />
* Levi B, Werman MJ. ''Long-term fructose consumption accelerates glycation and several age-related variables in male rats.'' J Nutr 1998;128:1442-9. [http://www.nutrition.org/cgi/content/full/128/9/1442 Fulltext]. PMID 9732303.
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*Barasi, Mary E. 2003. ''Human Nutrition: A Health Perspective'', 2nd edition. London: Arnold.
* McPherson JD, Shilton BH, Walton DJ. ''Role of fructose in glycation and cross-linking of proteins.'' Biochemistry 1988;27:1901-7. PMID 3132203.
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*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]  
* Higdon, J., Linus Pauling Institute, Oregon State U. [http://lpi.oregonstate.edu/infocenter/minerals/chromium/index.html ''Chromium'' 2003]
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*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]
* Wylie-Rosett,Judith, et al, ''Carbohydrates and Increases in Obesity: Does the Type of Carbohydrate Make a Difference?'' Obesity Research 12:124S-129S (2004)[http://www.obesityresearch.org/cgi/content/full/12/suppl_2/124S]
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*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, PJ, ''Dietary fructose: Implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism.'' Nutr Rev. 2005 May;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]
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*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.
* Bray, George A, ''Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity'' American Journal of Clinical Nutrition, Vol. 79, No. 4, 537-543, April 2004 [http://www.ajcn.org/cgi/content/full/79/4/537]  
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*Mann, Jim and A. Stewart Truswell, eds. 2002. ''Essentials of Human Nutrition'', 2nd edition. Oxford: Oxford University Press.
* Dennison, Barbara ''Excess Fruit Juice Consumption by Preschool-aged Children Is Associated With Short Stature and Obesity,'' PEDIATRICS Vol. 99 No.1, January 1997, pp. 15-22 [http://pediatrics.aappublications.org/cgi/content/full/99/1/15]
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*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==
 
==External links==
  

Revision as of 02:58, 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. However, these health trends have multiple contributing factors.

The chemical structure of fructose

The open-chain structure of fructose.

Fructose is a 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.

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.

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 as an energy source

Digestion and 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.

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 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.

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:

  1. The phosphorylation of fructose by the enzyme fructokinase to fructose-1-phosphate.
  2. A split of the six-carbon fructose into two three-carbon molecules, ‘’glyceraldehyde’’ and ‘’dihydroxyacetone phosphate’’ (an aldol cleavage).
  3. Glyceraldehyde is then phosphorylated by another enzyme so that it too can enter glycolysis.

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.

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 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 phosphates 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) is a deficiency of a fructose transporter enzyme in the enterocytes, 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.

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.

Sweetener consumption patterns

File:Usda sweeteners.jpg
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.

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 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] 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."[5]

References
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  1. 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.
  2. Jurgens, Hella and et al. (2005). Consuming Fructose-sweetened Beverages Increases Body Adiposity in Mice. Obesity Res 13: 1146-1156.
  3. 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.
  4. Sugar coated: We're drowning in high fructose corn syrup.
  5. 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

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