Exercise reshapes gut microbiota to ameliorate core symptoms in PCOS: molecular mechanisms and therapeutic implications

作者：Qianqian Li, Leqin Chen, Ronghui Wang · 发表于：Frontiers in Endocrinology · 年份：2025 · DOI：10.3389/fendo.2025.1652731 · 被引用次数：6 · 研究领域：Gut microbiota and health、Exercise and Physiological Responses、Cardiovascular and exercise physiology

Background: Polycystic ovary syndrome (PCOS) is a prevalent endocrine-metabolic disorder characterized by Insulin Resistance (IR), hyperandrogenism, and ovulatory dysfunction, with gut dysbiosis emerging as a key pathophysiological driver. Exercise, a non-pharmacological intervention, ameliorates PCOS symptoms, yet the molecular mechanisms linking exercise-induced gut microbiota remodeling to metabolic improvements remain elusive. Objective: This review synthesizes evidence on how exercise reshapes gut microbiota to reverse core PCOS pathologies through integrated molecular pathways. Results: ) and reduces pro-inflammatory pathogens (e.g., Proteobacteria), elevating short-chain fatty acids (SCFAs) and secondary bile acids (BAs) while suppressing lipopolysaccharide (LPS) translocation. We propose three core mechanisms:(1) SCFAs network reconstruction: Butyrate/propionate enhance gut barrier integrity (via ZO-1/Occludin), inhibit histone deacetylases (suppressing CYP17A1), activate GLP-1 secretion (FFAR3-dependent), and mitigate inflammation. (2) BA-FXR axis activation: Exercise increases secondary BAs (e.g., deoxycholic acid), activating hepatic FXR to inhibit gluconeogenesis (*PEPCK/G6Pase*) and upregulate androgen-clearance enzymes (*SULT2A1/CYP3A4*). (3) LPS-inflammation inhibition: Reduced LPS blunts TLR4/NF-κB signaling and NLRP3 inflammasome activation, resolving chronic inflammation. These axes converge to improve tissue-specific PCOS features: ovarian androgen synthesi...