Difference of Mechanism between Fructose-and Xylitol-induced Hyperuricemia
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We previously reported a practical procedure for evaluating the hyperuricemic effects of drugs by using rats treated with a urate oxidase inhibitor, potassium oxonate. Fructose and xylitol, which have hyperuricemic effects widely documented in clinical use, were useful model compounds for this assay method.<BR>However, the mechanisms by which the hyperuricemic effects were induced in the animals were not always the same. Fructose rapidly but transiently increased plasma uric acid in rats treated with potassium oxonate, while xylitol gradually increased it from at least two hours later. The increase of plasma uric acid caused by fructose followed an appreciable reduction of the hepatic ATP level, but xylitol caused no change in the hepatic adenine nucleotides during the duration of the hyperuricemic effect. Infusion of a high concentration of fructose solution for 15 min from the portal vein induced a more obvious decrease of the hepatic ATP level together with an apparent increase of plasma uric acid in arterial blood. Xylitol caused no such effects.<BR>Moreover, fructose obviously increased uric acid production in perfused rat liver by a cross-circulation technique with blood donor animals, but xylitol again had no effect. Both fructose and xylitol showed no appreciable effects on plasma and urinary uric acid levels in rats, in which the plasma uric acid level was maintained by treatments with allopurinol, potassium oxonate and exogenously administered uric acid.<BR>Accordingly, we concluded that both sugars showed hyperuricemic effects due to stimulation of uric acid production, but the mechanisms were obviously different. The hyperuricemic effect of fructose must be due to a rapid degradation of hepatic ATP as well documented by earlier workers, but that of xylitol may depend upon the stimulation of purine biosynthesis de novo.
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