The role of intestinal microbial metabolites in polycystic ovary syndrome: mechanistic insights and intervention prospects

Abstract

Background Polycystic ovary syndrome (PCOS) is a prevalent endocrine-metabolic disorder among women of reproductive age, defined by the core features of hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology. PCOS is frequently complicated by insulin resistance, obesity, dyslipidemia, and chronic low-grade inflammation, which substantially impair patients’ reproductive health, metabolic homeostasis, and quality of life. Although the etiology of PCOS remains incompletely elucidated, accumulating evidence indicates that gut microbiota and their metabolites participate in the pathogenesis and progression of PCOS via metabolic, immune, and neuroendocrine pathways. Focusing on the gut-ovary axis, this review systematically summarizes the molecular mechanisms by which gut microbial metabolites mediate PCOS-related pathological processes, as well as potential intervention strategies. Methods This article is a narrative review. To ensure comprehensive literature coverage, we searched the PubMed, Embase, Web of Science, and Cochrane Library databases from their inception to June 30, 2026. Search terms included polycystic ovary syndrome, PCOS, gut microbiota, gastrointestinal microbiota, microbial metabolites, short-chain fatty acids, bile acids, lipopolysaccharide, branched-chain amino acids, tryptophan metabolism, gut-ovary axis, probiotics, prebiotics, postbiotics, and fecal microbiota transplantation. Original basic research, clinical observational studies, randomized controlled trials, systematic reviews, meta-analyses, and clinical guidelines related to PCOS and gut microbiota were prioritized for inclusion. Content lacking clear support from primary literature, with evidence limited to other disease models, or involving excessive mechanistic extrapolation was either excluded or interpreted conservatively.