Gut Microbiota Modulation by Inulin Improves Metabolism and Ovarian Function in Polycystic Ovary Syndrome.

Summary

Inulin improved hyperandrogenism and glucose-lipid metabolism in a PCOS cohort and in mice, enriching SCFA-producing taxa and increasing fecal SCFAs. It lowered LBP and ovarian inflammation, effects that were abrogated by LPS, and benefits transferred via FMT from inulin-treated patients to mice.

Key Findings

• Inulin improved hyperandrogenism and glucose–lipid metabolism in both a PCOS patient cohort and mouse models.
• Inulin increased SCFA-producing taxa (e.g., Bifidobacterium; CAG12), enhanced SCFA biosynthesis capacity, and raised fecal SCFAs.
• Inulin reduced LBP and ovarian inflammation in PCOS mice; intraperitoneal LPS reversed these benefits.
• FMT from inulin-treated PCOS patients transferred improved insulin sensitivity, lipid handling/thermogenesis, and reduced hyperandrogenism/inflammation to recipient mice.

Clinical Implications

Prebiotic inulin may serve as an adjunct therapy in PCOS to improve insulin sensitivity, reduce hyperandrogenism, and attenuate ovarian inflammation, pending confirmation in randomized controlled trials and dose–response studies.

Limitations

• Non-randomized design with unspecified patient sample size and potential confounding in human cohort.
• Generalizability and durability of effects are unknown; dosing and formulation of inulin require optimization.

Future Directions

Conduct RCTs to define efficacy, dose–response, and responder phenotypes; integrate metabolomics and immune profiling to validate SCFA–LPS–ovarian inflammation pathways in humans.