FRUCTOSE

(C6H12O6)
History Fructose is a simple sugar that occurs naturally in foods. It gives fruits their sweet taste. Crystalline fructose obtained from processing corn or sugar is used in food and beverages as a nutritive sweetener. Its roughly 1.2 times the sweetness of table sugar in most food applications. Although originally marketed as a health supplement, crystalline fructose became available as a food ingredient about 20 years ago. G6P + NAD Phosphogluconate Fructose 6-Phosphate 6-Phosphate This kit is for the quantitative, enzymatic determination of fructose in food and other materials. Hexokinase Fructose + ATP Phosphate + ADP Fructose 6-

PGI Glucose

However, when compared to all other naturally occurring and added starches, syrups and sweeteners, fructose contributes only a small amount of calories to the average American diet.

G6PDH NADH + 6-

Fructose

is

phosphorylated

by

adenosine triphosphate(ATP) in the reaction catalyzed by hexokinase. Fructose 6-

phosphate is converted to glucose 6-

phosphate by phosphoglucose isomerase (PGI). Glucose-6-phosphate (G6P) is then oxidized to 6-phosphogluconate in the presence dinucleotide catalyzed dehydrogenase of nicotinamide (NAD) by in the adenine reaction

fructose delivery system theres nothing else to it, while fruit contains additional nutrients along with fibre, which affect digestion and absorption of the fructose. Plus, the amount of fructose in the average apple is much less than, say, the average can of soda. Fructose has a unique texture, sweetness, rate of digestion, and degree of absorption that is different from glucose, which is the sugar that most of our ingested dietary carbohydrates become when they hit the bloodstream.( Wasserman.L)

glucose-6-phosphate During this

(G6PDH).

oxidation, an equimolar amount of NAD is reduced to NADH. The consequent increase in absorbance at 340 nm is directly proportional to fructose concentration.

Review of Related Literature

High-fructose syrups (HFS) comprise fructose, dextrose, and minor amounts of

Fructose is a monosaccharide, the simplest form of carbohydrate. As the name implies, mono (one) saccharides (sugar) contain only one sugar group; thus, they cant be broken down any further. Each subtype of carbohydrate has different effects in the body depending on the structure and source (i.e. what food it comes from). The chemical structure affects how quickly and/or easily the carbohydrate molecule is digested/absorbed. The source affects

oligosacchanides. The predominant syrups of commerce contain 42% and 55%

fructose. HFS production was made possible by concurrent developments in refining, isomerization, and separation technologies in the 1960s. Fructose contributes many useful physical and functional attributes to food and beverage applications, including sweetness, flavor enhancement, humectancy, color and flavor development, freezing-point depression, and osmotic stability. HFS is used extensively in carbonated beverages, baked goods, canned fruits, jams and jellies, and dairy products. The use of crystalline fructose and crystalline fructose syrup have

whether other nutrients are provided along with the carbohydrate. For example, both high fructose corn syrup (HFCS) and fruit contain fructose, but their effects in the body are different. HFCS is essentially a simple

recently expanded from pharmaceutical and specialty food products to mainstream food and beverage applications.( Clin, ) J.,1993

Dietary fructose intake is increasing. It is increasing primarily from added sugars, including sucrose and high fructose corn syrup, and correlates epidemiologically with the rising prevalence of metabolic syndrome

Fructose is metabolized differently in the body than glucose is. Glucose is transported into the cells of the body by the hormone insulin, fructose is not3. Therefore, its ingestion does not stimulate insulin release. This, in turn, means that fructose ingestion does not lead to the insulin-induced rise in leptin. As an increase in insulin and leptin are associated with satiety, some researchers theorized that perhaps ingesting fructose instead of glucose leads people to consume more calories because they do not get the right signals to feel full. High fructose diets also have been shown to lead to a more direct formation and storage of fat5.

and

hypertension

worldwide.

The

administration of fructose to animals and humans increases BP and the development of metabolic syndrome. These changes occur independently of caloric intake

because of the effect of fructose on ATP depletion and uric acid generation. Fructose ingestion may also be a risk factor for kidney disease that includes glomerular hypertension, renal inflammation, and

tubulointerstitial injury in animals. It suggest excessive fructose intake

Experimental Related

Additionally, despite not having the same impact on insulin secretion as glucose, fructose ingestion is strongly tied to the development of insulin resistance and TypeII Diabetes. This appears to occur because ingestion of a high fructose diet leads to more fat production, including increased production of circulation triglycerides (a kind of fat) Utilization Of Fructose by E.coli There are three main routes for the utilization of fructose by Escherichia coli. One (Route A) predominates in the growth of wild-type strains. It involves the

functioning of the phosphoenolpyruvate: glycose phosphotransferase system (PTS) and a fructose operon, mapping at min. 48.7, containing genes for a membrane-spanning protein (fruA), a 1-phosphofructose kinase

(fruK) and a diphosphoryl transfer protein (fruB), under negative regulation by a fruR gene mapping at min. 1.9. A second route (Route B) also involves the PTS and membrane-spanning proteins that recognize a variety of sugars possessing the 3,4,5-Darabino hexose configuration but with primary specificity for mannose (manXYZ), mannitol (mtlA) and glucitol (gutA) and which, if over-produced, can transport also fructose.m A third route (Route C),

potentially

successful

diet

therapy

in

patients with irritable bowel syndrome and fructose malabsorption. Tables detailing the content of fructose and fructans in foods were constructed. A dietary strategy

comprising avoidance of foods containing substantial free fructose and short-chain fructans, limitation of the total dietary fructose load, encouragement of foods in which glucose was balanced with fructose, and coingestion of free glucose to balance excess free fructose was devised. Sixty-two consecutively referred patients with irritable bowel syndrome and fructose malabsorption on breath hydrogen testing underwent dietary instruction. Dietary adherence and effect on abdominal symptoms were

functioning in mutants devoid of Routes A and B, does not involve the PTS: fructose diffuses into the cell via an isoform (PtsG-F) of the major glucose permease of the PTS and is then phosphorylated by ATP and a manno(fructo)kinase (Mak+) specified by a normally cryptic 1032 bp ORF (yajF) of hitherto unknown function (Mak-o),

evaluated via telephone interview 2 to 40 months (median 14 months) later. Response to the diet was defined as improvement of all symptoms by at least 5 points on a _10to 10-point scale. Forty-eight patients (77%) adhered to the diet always or frequently. Forty-six (74%) of all patients responded positively in all abdominal symptoms.

mapping at min. 8.8 and corresponding to a peptide of 344 amino acids. Conversion of the Mak-o to the Mak+ phenotype involves an A24D mutation in a putative regulatory region

Fructose Malabsorption Dietary fructose induces abdominal symptoms in patients with fructose

Positive response overall was significantly better in those adherent than nonadherent (85% vs 36%; P_0.01), as was improvement in individual symptoms (P_0.01 for all symptoms). This comprehensive fructose malabsorption dietary therapy achieves a

malabsorption, but there are no published guidelines on its dietary management. The objective was to retrospectively evaluate a

high level of sustained adherence and good symptomatic response.

down before it reaches the rate-limiting enzyme (phosphofructokinase), thereby

supplying the body with an unregulated source of three-carbon molecules. These Different Sugars and Metabolism molecules are transformed into glycerol and fatty acids, which are eventually taken up by High Fructose Corn Syrup-55, which is commonly used in processed food and drinks, is 55% fructose, 42% glucose and 3% higher saccharides . Given that sucrose is a disaccharide, which is metabolized to one fructose and one glucose molecule it has been argued that there is little difference between fructose and sucrose, since both provide about 50% fructose and 50% glucose in the blood stream; and until recently, there was no evidence that HFCS contributes to long-term weight gain beyond what sucrose contributes. However, the present study suggests that HFCS and sucrose can have different effects on body weight and obesigenic measures. HFCS is different than sucrose in many ways. First, HFCS-55 has proportionately slightly more fructose than sucrose. Second, fructose is absorbed further down the intestine than glucose, with much of the metabolism occurring in the liver, where it is converted to fructose-1-phsophate, a precursor to the backbone of the triglyceride molecule. Third, fructose is metabolically broken Fructose is sweeter than table sugar so less is needed to attain the similar sweetness, offering calorie savings. Fructose has a low down Glycemic Index, which is Conclusion adipose tissue, leading to additional

adiposity. And fourth, HFCS causes aberrant insulin functioning, in that it bypasses the insulin-driven satiety system. Whereas

circulating glucose increases insulin release from the pancreas, fructose does this less efficiently, because cells in the pancreas lack the fructose transporter. Typically, insulin released by dietary sucrose inhibits eating and increases leptin release, which in turn further inhibits food intake. As

previously discussed, meals of HFCS have been shown to reduce circulating insulin and leptin level. Thus, fructose intake might not result in the degree of satiety that would normally ensue with a meal of glucose or sucrose, and this could contribute to increased body weight.

useful in formulating foods with a low Glycemic Load. Crystalline fructose offers unique benefits when use in a variety of foodstuffs, as well as enhanced product quality, savor and stability. On the other hand fructose, if intake too much will be detrimental to human health such as Fructose malabsorption. For

References y Elliott SS, Keim NL, Stern JS, Teff K, and Havel PJ.2002. Fructoseweight gain, and the insulin resistance syndrome. Am. J. Clinical Nutrition. 76: 911 - 922. Johnson,R.j.,Sanchez-Lozada, G.,and Nakagawa,T.,2010. The Effect of Fructose on Renal Biology and Disease. J Am Soc Nephrol 21: 1046-6673/2112 Kornberg, H.L.2001. Routes for Fructose Utilization by Escherichia coli.J. Mol. Microbiol. Biotechnol.3(3): 355-359. Sheperd,S.J.,GibsonP.2006. Fructose Malabsorption and Symptoms of Irritable Bowel Syndrome: Guidelines for Effective Dietary Management. J Am Diet Assoc.106:1631-1639. Wasserman,L.(n.d). Fructose is a Simple Sugar.Retrieved from http://bodybasicsbootcamps.homeste ad.com/bonuses/Fructose_vs_Glucos e.pdf