Gout and type 2 diabetes mellitus (T2DM) are prevalent metabolic disorders with a significant bidirectional association. The review article focuses on the interplay between serum uric acid and glucose/lipid metabolism, innate immunity, inflammation, and gut microbiota, proposing simultaneous treatment strategies. Gout, caused by monosodium urate crystal deposition due to hyperuricaemia, and T2DM, induced by high-fat, high-sugar diets disrupting metabolic balance, share common pathological mechanisms. Elevated uric acid levels contribute to lipid and glucose metabolic disorders, activate inflammatory pathways like the nucleotide-binding oligomerization domain-like receptor 3 inflammasome, and trigger innate immune responses. The gut microbiota also plays a significant role in both metabolic diseases, with dysbiosis affecting uric acid excretion and insulin resistance. This review article highlights promising therapeutic approaches, including the use of sodium-glucose cotransporter-2 inhibitors which reduce serum uric acid and lowers gout risk alongside glycaemic control. Additionally, targeting inflammatory pathways such as interleukin-1β offers potential benefits for both conditions. Combined pharmacological therapies, dietary adjustments, and gut microbiota interventions present new directions for simultaneous management. This review article provides a comprehensive analysis of the links between gout and T2DM, offering novel insights for clinical practice and future research.
Wang et al. (Wed,) studied this question.