| Sumario: | Hyperuricemia (HUA) has become the fourth most important health-threatening risk factor after hypertension, hyperglycemia, and hyperlipidemia, but the efficacy of existing uric acid-lowering treatments (ULT) is poor, and there is an urgent need to explore novel ULT strategies. <i>Akkermansia muciniphila</i> (<i>A. muciniphila</i>), a next-generation probiotic, shows promise in promoting intestinal homeostasis and metabolic regulation. Previous studies have demonstrated the potential application of <i>A. muciniphila</i> in ULT, but its specific mechanism has not been elucidated. In this study, we isolated a strain of <i>A. muciniphila</i>, named K101, from the cecum of goslings. In vitro experiments showed that K101 directly degrades uric acid, suggesting a potential microbial-metabolic crosstalk mechanism for anti-HUA. In vivo experiments showed that K101 increased the abundance of uric acid metabolism-related microbiota, such as <i>A. muciniphila</i> and <i>Lactobacillus</i>. Functionally, K101 synergistically promoted uric acid excretion by activating the intestinal excretory protein ABCG2 and inhibiting the renal uric acid reabsorption protein GLUT9. In addition, K101 provides a stable environment for uric acid metabolism by inhibiting renal inflammatory responses. Overall, <i>A. muciniphila</i> K101 exerts anti-HUA effects by remodeling the intestinal microbiota and excretion of uric acid through the gut-renal axis. This study offers new insights into microbial-metabolic crosstalk in uric acid metabolism in <i>A. muciniphila</i> and identifies potential targets for gout prevention and ULT strategy development.
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