Fig. 3.

Potential deleterious effects of fructose-induced hyperuricemia. Fructose may increase plasma uric (i.e., hyperuricemia) acid through (1) transient intrahepatocellular energy depletion (due to ATP consumption by fructokinase following large i.v. fructose loads), (2) stimulation of endogenous uric acid synthesis from purine and glycine precursors (by unknown mechanisms), and (3) decreased uric acid excretion (by competition with lactate for secretion into urinary tubules). In turn, hyperuricemia may contribute to the metabolic effects of fructose by triggering inflammation through the NALP3 inflammasome or by impairing endothelial function, in turn promoting insulin resistance and hypertension. Hyperuricemia may also activate lipogenic enzymes (not shown). ATP adenosine triphosphate, Fructose-1-P fructose-1-phosphate