Weizmannia coagulans BC99 alleviates hyperuricemia by restoring liver–kidney–gut axis dysfunction caused by hyperuricemia

Abstract

Hyperuricemia (HUA) has emerged as a global metabolic disorder that poses significant risks to human health. To investigate the effects and mechanisms of Weizmannia coagulans BC99 in alleviating hyperuricemia, we established a hyperuricemia mouse model. The results demonstrate that BC99 significantly downregulates the expression of uric acid (UA) reabsorption proteins in the kidneys and intestines, while upregulating the expression of UA excretion proteins. This modulation leads to a reduction in UA synthesis, mediated through the Nrf2/NLRP3 pathway. Additionally, BC99 intervention restored gut microbiota intestinal dysbiosis in HUA mice, increased the beneficial short-chain fatty acid (SCFA)-producing bacterial genera, and corrected disturbances in amino acid, purine, and pyrimidine metabolism. Collectively, our findings suggest that BC99 exhibits strong anti-hyperuricemic effects and holds promise as a dietary supplement for lowering uric acid levels.