Abstract
This review presents recent data on direct and indirect pathogenetic relationships between metabolism of purine compounds and biochemical processes in cells of the digestive system. A comprehensive analysis of available modern publications for the period from 2000 to 2022 in the Scopus, PubMed, eLIIBRARY, and Google Scholar databases was performed. The hypothesis linking the pathogenesis of hyperuricemia to “renal overload” suggests that the disease may develop due to impaired renal excretion with insufficient excretion of uric acid (UA) via the intestine. Some of the UA transport systems work actively in hepatocytes and enterocytes, which determines their formation and excretion. UA transporter proteins are divided into two categories: urate reabsorption transporters and urate excretion transporters; their expression is regulated by transcription factors, hormones, and metabolites of the intestinal microflora. The influence of intestinal microbiota on UA metabolism is associated with its involvement in purine metabolism, degradation and excretion of UA together with metabolites of intestinal flora, and suppression of gout inflammation, and is evaluated as a new therapeutic potential for gout and hyperuricemia to prevent renal damage and urolithiasis.
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