Fecha de publicación: -- Fuente: PubMed "microbial biotechnology" Sci China Life Sci. 2026 Nov 4. doi: 10.1007/s11427-026-3560-6. Online ahead of print.ABSTRACTIn this study, supplementation with Panax notoginseng (PN) in obese mice reversed excessive weight gain, improved glucose homeostasis and insulin sensitivity, and significantly reversed hepatic steatosis. Concurrently, PN treatment normalized the intestinal microecosystem, reflected in a decreased Firmicutes-to-Bacteroidetes ratio (F/B ratio) and an enrichment of the commensal species Enterocloster clostridioformis (EC). Of particular note, oral administration of EC alone largely reproduced the major beneficial phenotypes observed with PN-namely, reduced fat mass, improved glycaemic regulation, and attenuated hepatic triglyceride deposition. Mechanistically, EC intervention suppressed the pathological overactivation of the hepatic insulin receptor substrate (IRS)-phosphatidylinositol-3 kinase (PI3K)-AKT kinase (AKT) pathway and inhibited the phosphorylation of IRS. This recalibration of the insulin signaling cascade improved insulin sensitivity and effectively counteracted the metabolic disturbances provoked by the high-fat diet (HFD). Taken together, these results suggest that the anti-obesity effects of PN are at least partially mediated by gut microbiota-driven EC enrichment, with consequent modulation of the IRS-PI3K-AKT pathway. Collectively, our findings identify EC as a potential candidate commensal bacterium and highlight the importance of the PN-EC-IRS-PI3K-AKT regulatory axis in counteracting obesity and its associated comorbidities.PMID:43000596 | DOI:10.1007/s11427-026-3560-6