Abstract
The hyperuricaemia following fructose loading was first demonstrated by Perheen-tupa and Raivio in 1967 (1). Subsequent studies (reviewed in 2) established that this elevation of plasma and urine uric acid concentrations in humans followed the rapid degradation of hepatic ATP used in the fructokinase reaction (Fig. 1). Experiments in rats given a parenteral fructose load showed that the hepatic concentration of ATP fell by 40% within 2 min, followed by an equivalent rise in ADP and AMP (3). These changes were accompanied by severe Pi depletion due to rephosphorylation of ADP in the mitochondria and were confirmed subsequently by NMR spectroscopy in humans (2). Further catabolism of AMP proceeded via AMP deaminase (AMPDA). AMPDA is normally activated by ATP, and strongly inhibited by GTP and Pi. The rapid fall in both the latter following fructose loading released these normal physiological controls, with the accumulation of IMP which was then further degraded via inosine by purine nucleoside phosphorylase (PNP) to hypoxanthine (Fig. 1). Rapid conversion of hypoxanthine to xanthine and uric acid followed because of the high activity of xanthine dehydrogenase in human liver.
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