The human gut microbiota and uric acid metabolism: genes, metabolites, and diet

Hyperuricemia (HUA), characterized by an excessive production of uric acid (UA), poses a significant risk for various metabolic disorders and affects over one billion individuals globally. The intricate interplay between the gut microbiota and dietary constituents plays a pivotal role in maintaining UA homeostasis. Abnormal consumption of specific dietary components such as purines, fructose, or aberrant expression of urate transporters can disrupt UA balance, precipitating HUA and gout. The gut microbiota exerts profound influence over human UA regulation, particularly in the presence of specific gene clusters. Individuals with HUA often exhibit gut dysbiosis, characterized by a reduction in bacteria producing short-chain fatty acids or those capable of degrading UA, alongside an increase in opportunistic pathogens. Dietary constituents and their microbial metabolites engage in intricate interactions with the gut microbiota to modulate HUA, regulating inflammatory responses, suppressing xanthine oxidase activity to curtail UA production, and enhancing UA excretion via urate transporters. This comprehensive review delineates the pivotal role of dietary factors in UA metabolism and HUA, elucidating the underlying mechanisms of microbial regulation. By unraveling the intricate connections between the gut microbiota and UA metabolism, it offers valuable dietary guidance for individuals grappling with HUA.