Fructose

• D-(- ) -fructose
• Levulose
• Levulose
• L, D, D- ketohexose
• α - acrose

• 57-48-7 ( D-( -)- fructose)
• 7776-48-9 ( L-( )- fructose)
• 6035-50-3 (DL- (±)- fructose)

V06DC02

Colorless and odorless, very sweet tasting prisms or needles

Fixed

1.59 g · cm -3

100-104 ° C

• Well in water: 790 g · l-1 (at 20 ° C)
• Soluble in acetone, moderately in ethanol, badly in diethyl ether, benzene and chloroform

Template: Infobox chemical / molecular formula search available

Fructose ( fruit sugar colloquially, often fructose, from Latin fructus, fruit ', outdated levulose ) is a naturally occurring chemical compound with the molecular formula C6H12O6. Fructoses include monosaccharides ( simple sugars ) to carbohydrates. It occurs in several isomeric ( anomeric ) forms. In this article, the information concerning the physiology alone the D- fructose. L-fructose has no physiologically and otherwise of little importance.

• 6.1 Fehling's test
• 6.2 Seliwanow sample

Occurrence

Fructose is found in nature mainly in fruits such as pome fruit (apples and pears, each about 6 g/100 g), berries (such as grapes 7.5 g/100 g), and in some exotic fruits ( pomegranate and persimmon ) and in honey before ( 35.9 to 42.1 g/100 g). In table sugar (made from sugar beets or sugar cane ) is fructose contained in bound form: cane or beet sugar (sucrose ) is a disaccharide consisting of one molecule of glucose (dextrose ) and fructose is composed. A significant share of the sugar intake comes from industrially manufactured foods enriched with fructose syrup from corn starch (high - fructose corn syrup, HFCS) contained.

Properties

Fructose is a colorless, odorless, readily soluble in water, very sweet-tasting compound that forms prismatic or acicular, highly hygroscopic crystals. At 60 % humidity, it takes within one hour, 0.28 % water, 0.6 % within 9 days. The monosaccharide is optically active and therefore exists in two spiegelbildichen isomers, called enantiomers. Fructose belongs to the hexoses and - because of the keto group - to the ketoses. In crystalline form it is a six-membered ring in front ( fructopyranose ) bound as five-membered ring ( fructofuranose ).

The α - and β - anomers of the respective ring shapes can be transformed into each other in aqueous solution and communicate with each other in equilibrium. At 20 ° C is dissolved in water, D- fructose to 76 % in the β - pyranose form, to 4 % in the α - furanose and 20% in the β - furanose ago.

Industrial use and displacement

For economic and logistical reasons, namely convenient transportation by tanker and the opposite table sugar 20 % higher sweetening power of fructose, an increasing displacement of other sweeteners can be observed. Be seen that the sugar beet area goes back, and sugar factories ( Regensburg, Groß Munzel, United Gerau, etc.) will be closed, which is under the light of reducing subsidies to do with increasing import of cane sugar. On the other hand, increased sales opportunities (eg E10 gasoline) as part of the general introduction of bio-fuels through the use of bio-ethanol in the fuel sector. The EU sugar regime provides for a reduction in the volumes of table sugar, but at an annual rate of 100,000 tonnes of isoglucose ( = HFCS) for a stock of 500,000 tons in 2007.

Physiology

In the intestine, fructose is from people of good, especially slower than glucose, absorbed. This is due to the passive transport through specific proteins, for a through the so-called GLUT5 ( apical, i.e. the intestinal lumenal cell surface ), the fructose granted access to the intestinal cells ( enterocytes ), and secondly by GLUT2 (basolateral, i.e., bloodstream faces ) that allows fructose to enter the blood of the intestine cells. Glucose, however, is secondary - active ( SGLT1, apical), thus consuming energy, is pumped into the cell. This is regulated by a feedback inhibition. In contrast, fructose unregulated flows without expenditure of energy along its concentration gradient. This means that fructose is not completely received from the food. Thus consists primarily in young children is a risk that it comes at too high Fructosemengen in the diet to osmotic diarrhea.

D-fructose is converted by the enzyme Ketohexokinase into D-fructose -1 - phosphate in the cells of the liver, it can not leave the cell. The supply of energy-rich phosphates is " plundered " by the Ketohexokinase: ATP → ADP → upregulated AMP and AMP deaminase. It falls on the IMP, the concentration of uric acid can rise above the Purinabbau. Fructose -1-phosphate is divided by fructose-1 -phosphate aldolase conveyed into dihydroxyacetone phosphate and glyceraldehyde. After phosphorylation of glyceraldehyde can enter the glycolysis (as glyceraldehyde -3-phosphate then ). More significant is the outflow of the decay products in the triglyceride synthesis. Triglycerides stored as fat deposits, but also as fat droplets between myofibrils of muscle. In adipose tissue fructose can also occur as fructose-6 -phosphate in the glycolysis, when the glycogen stores are depleted.

Synthesis

The body is fructose prepared by the so-called Polyolweg from glucose ( locally, for example in the seminal vesicles in males as a nutrient for the spermatozoa ), wherein the glucose is reduced, together with the co-substrate NADPH to sorbitol, which is then oxidized to fructose by sorbitol dehydrogenase where NAD is reduced to NADH. Net leads to a conversion of NADPH to NADH, which is held responsible for some of the long-term consequences of chronic high blood glucose levels (e.g., diabetes ), as NADPH is required by the cell and for the detoxification of hazardous oxygen compounds in elevated glucose levels in the However, more blood glucose is converted to fructose via Polyolweg so that more NADPH consumed. In addition, fructose and sorbitol accumulate in the cells, which on the one hand the cell osmotically damaged and whereas certain cellular enzymes are inhibited by high concentrations of these two sugars.

Pathophysiology

In humans, disorders of fructose absorption in the intestine or of fructose metabolism in the liver to cause disease symptoms. Clinical significance of the frequent fructose malabsorption (also intestinal fructose called ), in which a disturbed Fructose transport is assumed by the intestinal cells, and the rare but leading to serious symptoms, Hereditary fructose intolerance ( HFI ) which is determined by an inherited disorder of fructose metabolism the liver is due, in fructose can not be broken down in sufficient quantities or not.

Estimated 30-40% of Europeans have the fructose malabsorption, with about half showing symptoms. The disorder occurs predominantly in childhood. Nichtresorbierter fructose is broken down by the bacteria of the intestinal flora predominantly anaerobically to carbon dioxide, hydrogen and short-chain fatty acids. These produce irritable bowel symptoms such as bloating, abdominal pain, mushy, sometimes foul-smelling stool and diarrhea. Hereditary fructose intolerance is much less common; to approximately 130,000 healthy people is a HFI of the stakeholders. This form of fructose intolerance caused by a disorder of glucose metabolism a dangerous blood sugar (hypoglycaemia ).

Use as a sweetener

For a long time it was recommended to sweeten foods dietary fructose. In relation to sucrose (ie, table sugar ) has a 10 percent D- fructose sweetening power of 114 percent. The blood sugar rises on supply of fructose significantly slower than for supply of sucrose commonly used in the kitchen; the glycemic index is 20 on a fairly low level. ( Note for people with diabetes and insulin therapy: This description is not usually carried fruit / fruit ingested fructose talk fruit belongs to the to be calculated carbohydrates ( KH) For example, is an orange one carbohydrate unit ( KE), the. . the blood glucose as compared to other meals increases rapidly. )

However, the Federal Institute for Risk Assessment ( BfR) in her analysis of existing studies concluded that the continued use of fructose as a sugar substitute in industrially produced foods as part of so-called diabetic foods instead of commercial sucrose from diet- medical point of view does not make sense, since there was an increased fructose intake has an adverse effect on the metabolism and also an excess of fructose in the diet favors the development of obesity and the metabolic syndrome.

After work of the group to Richard J. Johnson leads the supply of fructose - as well as of ethanol - the rise in uric acid, which due to the lack of uricase in the great apes ( hominids ) show significantly worse impact than in, for example, laboratory rats: in vascular endothelium is a decreased bioavailability of the Second ( NO) determine messenger nitric oxide, which can cause stiffening of the vessel wall and thus explain high blood pressure. Since NO must be available for the effect of insulin on the insulin receptor, is an insulin resistance in NO deficiency.

Genesis of obesity ( obesity )

According to a study by the German Institute of Human Nutrition, which was conducted in mice, there is a relationship between Fructosekonsum and overweight, which is not due to an increased calorie intake, but to an influence of the fat and carbohydrate metabolism. In fact, people could also be demonstrated in a study that fructose is converted into body fat much faster by the body as glucose. Moreover, the results of this study indicate that a fructose intake stimulates lipogenesis (fat synthesis) and the storage of fats from the diet increases. Moreover, the use of fructose seems to lead to a lower satiety, as these does not induce insulin secretion and insulin is also one of the satiety hormones.

Genesis of diabetes

In the United States the commercial use of fructose increased in the 1970s drastically - the consumption of high fructose corn syrup ( HFCS), a particularly high fructose corn syrup version, rose from 0.23 kg per person per year in 1970 to 28.4 kg per person per year in 1997. HFCS is used in the United States, particularly in soft drinks, wherein the fructose content of up to 90 % ( HFCS 90) is increased. This sweetener is particularly cost-effective for the manufacturer, since in the U.S. corn production is subsidized, whereas the sugar import must be cleared through customs. This significant change in the composition of the sugar to food additives made ​​without the potential effects on human metabolism previously studied extensively.

Improve According to a study by the group of MC Moore of Vanderbilt University ( Nashville, Tennessee), small amounts of fructose in healthy humans and in patients with type 2 diabetes mellitus, glucose tolerance and glycemic response without increased insulin secretion. In another study, participated for 5 weeks large quantities of fruit sugar in the subjects, a strong increase of cholesterol and triglycerides in the blood showed, but only in male subjects.

A diet enriched with fructose, results in animal studies to insulin resistance and obesity. Even for people was a associated with a high fructose diet significant decrease in insulin sensitivity are detected, and indeed much more than in a glucose- rich diet. The increase in consumption of fructose is brought pursuant to this effect with the increase of the metabolic syndrome, a risk factor for coronary heart disease, in context.

Genesis of liver cirrhosis

Recent research by Manal F. Abdelmalek and colleagues suggest further points out that not only the excessive consumption of alcohol, but also that of fructose containing beverages such as sodas and other sweetened soft drinks, damage to the liver through to fatty liver ( steatosis ) may result with concomitant pathological proliferation of the connective tissue (fibrosis). The rapidly increasing in recent years Fructosekonsum thus not only plays an important role in the development of metabolic syndrome, but is according to recent studies an independent risk factor for non- alcohol-related fatty liver disease ( nonalcoholic fatty liver disease ) dar.

Genesis of gout

Several prospective studies with several thousand subjects also suggest the suspicion that consumption of soft drinks and ( concomitantly ) fructose is strongly associated with the risk of gout ( Urikopathie ). Also fructose - rich fruits and fruit juices appear to increase the risk of developing gout, whereas in this respect there is no danger of diet sodas.

German legislation

§ 12 of the Regulation on dietary foods (so-called dietary regulation ) governed once the composition of special products for diabetics. Since October 1, 2010, this item is deleted because of the state of research on diabetic diets and sugar substitutes shows that these patients do not need such products, and that an increased Fructosekonsum may even have harmful effects on health ( see text). Fructose is the proprietary name of a type of sugar.

Proof

Fehling's test

As α - hydroxyketone fructose has a reducing effect, besides it can be converted (see ketol enediol tautomerism ), so that a balance between all of these isomers is present in an alkaline medium in mannose and glucose.

Seliwanow sample

The Seliwanow reaction is evidence of ketohexoses in the furanose ring form. Since it runs in an acidic environment, it does not come to ketol enediol tautomerization. With glucose, the sample falls therefore negative.

First, the fructose is heated with hydrochloric acid. This creates the 5-hydroxymethylfurfural. This then reacts with resorcinol to form a red precipitate.