Abstract
The rapid infusion of fructose is known to increase uric acid synthesis through consumption of ATP in fructose phosphorylation and conversion of AMP to IMP, cleavage of IMP, phosphorolysis of inosine, and oxidation of hypoxanthine and xanthine to uric acid. The congenital absence of xanthine oxidase provides an in vivo model further to elucidate the contribution of alternative pathways to fructose-induced hyperuricemia. Two brothers with hereditary xanthinuria were given a fructose infusion and the following was observed: (a) no change in the low levels of serum urate (0.4 and 0.6 mg/dl) and urinary uric acid (0.02 and 0.03 mmol/g creatinine) as compared to a control group who showed mean increases of 150 and 275 percent from the baseline values, respectively; (b) an increase in elevated baseline urinary xanthine from 1.7 and 1.3 to 2.7 and 1.8 mmol/g creatinine; (c) an elevation of plasma guanosine from undetectable values to 0.7 and 0.9 uM; and (d) an increase in the elevated plasma xanthine levels from 12.4 and 6.8 uM to 18.0 and 16.1 uM, as compared to a mean baseline value of 0.8 and increase to 3.6 uM in controls. These data suggest that GTP degradation contributes to fructose-induced hyperuricemia.
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Mateos, F., Puig, J., Ramos, T. et al. EFFECT OF FRUCTOSE INFUSION IN HEREDITARY XANTHINURIA EVIDENCE FOR GTP DEGRADATION: 127. Pediatr Res 19, 765 (1985). https://doi.org/10.1203/00006450-198507000-00147
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DOI: https://doi.org/10.1203/00006450-198507000-00147