Fructose metabolism affected

Besides hypoglycemia, D-fructose-induced renal acidification in the HFI defect involves a lowered hydrogen-ion secretory capacity of the proximal nephron, as evidenced by a 20 to 30% diminution in renal-tubular (T) reabsorption of bicarbonate (THCO3) and simultaneous occurrence, and persistence throughout D-fructose administration, of impaired tubular reabsorption of phosphate, cc-amino nitrogen, and uric acid. This abnormality of renal metabolism affects the renal cortex, which contains aldolase B, but does not affect the renal medulla. Thus, the abnormality may result from accumulation of D-fructose 1-phosphate in the renal cortex. The intimate, biochemical mechanism for renal, tubular acidosis is still unknown.164... 

NADPH balances are often essential for metabolite balancing based estimations of the net fluxes in a metabolic network. However, NADPH consumption and generation are often found in bidirectional reactions that cannot be quantified by metabolite balancing approaches. The mannitol cycle (Fig. 9) is an example of a pathway that can affect the NADPH balance, but has no net conversion of any metabolites, except for cofactors. In the mannitol cycle, NADH and NADP+ are converted into NAD+ and NADPH, respectively, at the expense of ATP [52]. Because mannitol happens to be symmetrical, the activity of the mannitol cycle will cause scrambling of the carbon atoms of fructose 6-phosphate, and the activity of the cycle may therefore be identified using labeling analysis. The mannitol cycle has been reported to be present in several fungi [52]. 

AT-Acetyl-D-glucosamine 6-phosphate is metabolized to the D-fructose ester more slowly (by preparations of kidney enzyme) than is D-glucosamine 6-phosphate/ Acetate inhibits the disappearance of AT-acetyl-n-glucos-amine 6-phosphate, but does not affect the disappearance of D-glucosamine 6-phosphate. A possible sequence of reactions for these transformations is as follows. ... 

Important disaccharides include lactose and sucrose. Lactose is a disaccharide of p-D-galactose bonded p(l 4) with D-glucose. In galactosemia, defective metabolism of galactose leads to accumulation of a toxic by-product. The ill effects of galactosemia are avoided by exclusion of milk and milk products from the diet of affected infants. Sucrose is a dimer composed of a-D-glucose bonded (al —> p2) with p-D-fructose. 

The dangers of consuming HFCS are apparent for at least one group of people, those who lack the enzyme needed to metabolize fructose properly. Individuals with this genetic disorder may develop serious reactions if exposed to even a very small amount of fructose, reactions that include sweating, nausea, vomiting, confusion, abdominal pain, and, in extreme cases, convulsion and coma. Fortunately, this disorder is quite rare, affecting one person in about every twenty thousand individuals. For those with the disorder, however, care must be used in the kinds of sweeteners included in the diet. 

Glucose easily penetrates the blood-brain barrier of nephrectomized and eviscerated animals, but its distribution in the brain is not affected by insulin. Fructose and ribose do not pass the brain-blood barrier at all. Yet fructose is a good substrate for brain hexokinase and is metabolized in brain homogenates. From the observations made in vitro, fructose seems to be a good substrate for brain metabolism in vivo. But such an interpretation is false since direct in vivo experiments have shown that fructose cannot enter the brain. 

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