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Hypothesis: fructose-induced hyperuricemia as a causal mechanism for the epidemic of the metabolic syndrome

The increasing incidence of obesity and the metabolic syndrome over the past two decades has coincided with a marked increase in total fructose intake. 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. Consistent with this hypothesis is the observation that changes in mean uric acid levels correlate with the increasing prevalence of metabolic syndrome in the US and developing countries. In addition, we observed that a serum uric acid level above 5.5 mg/dl independently predicted the development of hyperinsulinemia at both 6 and 12 months in nondiabetic patients with first-time myocardial infarction. Fructose-induced hyperuricemia results in endothelial dysfunction and insulin resistance, and might be a novel causal mechanism of the metabolic syndrome. Studies in humans should be performed to address whether lowering uric acid levels will help to prevent this condition.



Metabolism  Volume 21, Issue 8August 1972, Pages 713-721

Studies on the mechanism of fructose-induced hyperuricemia in man

Irving Fox and William Kelley


The rapid intravenous infusion of fructose produces a transient increase in plasma urate concentration, as well as an increase in the urinary excretion of oxypurines and uric acid. Fructose-induced hyperuricemia and hyperuricaciduria is associated with a striking increase in the blood lactate concentration, a decrease in erythrocyte phosphoribosylpyrophosphate (PP-ribose-P) and ribose-5-phosphate concentration, and no detectable change in erythrocyte ATP concentration. Although pretreatment with allopurinol prevents the hyperuricemic effect of fructose, the increase in plasma lactate is not modified and the increase in urinary oxypurine excretion is enhanced. These results are consistent with the hypothesis, based on previous studies in the rat, that fructose-induced hyperuricemia in man results from an increased degradation of purine ribonucleotides.

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