FRUCTOSE INDUCED HYPERURICEMIA PDF

Metrics details Abstract Extract: After the infusion of fructose, 0. The mean blood inorganic phosphate Pi levels were significantly less than the mean fasting value after fructose. Blood glucose, lactic acid, and fructose levels were significantly increased after fructose, but serum magnesium levels did not change. In two patients with hereditary fructose intolerance HFI the peak blood uric acid levels were The serum Pi level decreased 2.

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Metrics details Abstract Extract: After the infusion of fructose, 0. The mean blood inorganic phosphate Pi levels were significantly less than the mean fasting value after fructose. Blood glucose, lactic acid, and fructose levels were significantly increased after fructose, but serum magnesium levels did not change.

In two patients with hereditary fructose intolerance HFI the peak blood uric acid levels were The serum Pi level decreased 2. The mean uric acid excretion, expressed as milligrams per mg urinary creatinine, was 0. In two patients with HFI the uric acid excretion increased four- to fivefold after fructose administration; the increased uric acid excretion in HFI exceeded that of normal children.

In three patients with galactosemia, increases in blood uric acid levels after galactose ingestion were similar to those in normal children after fructose, but less than those in patients with HFI after fructose. The serum Pi levels decreased less in galactosemic patients after galactose administration than in patients with HFI after fructose infusion. These studies support the hypothesis that fructose-induced hyperuricemia results from degradation of adenosine monophosphate.

This effect appears to be specific for fructose. The lack of hyperuricemia in galactosemia patients after galactose ingestion may be explained by the observation that galactose is phosphorylated more slowly than fructose.

Speculation: Fructose administration in individuals predisposed to hyperuricemia and gout may induce urate overproduction by decreasing intrahepatic Pi and ATP content and ultimately lead to enhanced nucleotide catabolism. The pathogenesis of increased urate production in glycogen storage disease, type I, may be similar to that proposed for fructose-induced hyperuricemia.

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Fructose-Induced Hyperuricemia Is Associated With a Decreased Renal Uric Acid Excretion in Humans

Epub Nov Lactobacillus brevis DM ameliorates fructose-induced hyperuricemia through inosine degradation and manipulation of intestinal dysbiosis. Electronic address: vivianmarat Probiotics are powerful weapons to combat metabolic disturbance and intestinal dysbiosis. Previously we isolated a Lactobacillus strain named DM that could reduce the serum uric acid UA level by assimilating purine nucleosides. The present study aimed to evaluate the effects of DM on high-fructose-induced hyperuricemia and to elucidate the underlying mechanisms. Metabolic parameters, fructose- and UA-related metabolites, and fecal microbiota were investigated.

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Studies on the mechanism of fructose-induced hyperuricemia in man.

Pediatr Res. Fructose-induced hyperuricemia: observations in normal children and in patients with hereditary fructose intolerance and galactosemia. After the infusion of fructose, 0. The mean blood inorganic phosphate Pi levels were significantly less than the mean fasting value after fructose.

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Fructose-induced hyperuricemia is associated with a decreased renal uric acid excretion in humans.

Nat Clin Pract Nephrol. Hypothesis: fructose-induced hyperuricemia as a causal mechanism for the epidemic of the metabolic syndrome. Fructose--unlike other sugars--causes serum uric acid levels to rise rapidly. We recently reported that uric acid reduces levels of endothelial nitric oxide NO , a key mediator of insulin action. NO increases blood flow to skeletal muscle and enhances glucose uptake.

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