Multi-omics strategies combined with molecular docking to explore the regulatory effects of licochalcone A on glycolipid metabolism in db/db mice

. The combined analysis of liver metabolomics and liver proteomics indicated that LicA altered the intestinal microbiota metabolite hypotaurine through p-75-a5, and hypotaurine played a bridging role between p-75-a5 and glycolipid metabolism in T2DM. Through multi-omics joint analysis and WB experimental verification, the results showed that LicA activates the PPAR signaling pathway to improve glucose lipid metabolism disorders in T2DM. More importantly, after treating db/db mice with antibiotics, the beneficial effects of LicA were blocked, indicating that the gut microbiota plays a key role in LicA's improvement of glucose and lipid metabolism in T2DM. In conclusion, this study revealed a new mechanism by which LicA improves T2DM glucose and lipid metabolism disorder, and the potential improvement of LicA's glucose and lipid metabolism in T2DM may be related to the change of p-75-a5 targeting hypotaurine.