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.
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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. Whole-genome sequencing of strain DM was also conducted.
In addition, an inosine hydrolase from DM was heterologously expressed in Escherichia coli, and its inosine-degrading activity was detected. It could protect against high-fructose-induced liver damage and retard UA accumulation by degrading inosine.
The modulation effect of DM on high-fructose-induced intestinal dysbiosis resulted in enhancement of intestinal barrier function and reduction of liver lipopolysaccharide, which was closely correlated with the down-regulation of inflammatory cytokine-stimulated xanthine oxidase expression and activity.
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Studies on the mechanism of fructose-induced hyperuricemia in man.
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.
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. Animals deficient in endothelial NO develop insulin resistance and other features of the metabolic syndrome. As such, we propose that the epidemic of the metabolic syndrome is due in part to fructose-induced hyperuricemia that reduces endothelial NO levels and induces insulin resistance.