Bile acid metabolism: a potential node in the pathogenic network of PCOS
Polycystic ovary syndrome (PCOS) is a common disorder among women of reproductive age, characterized mainly by metabolic and endocrine disturbances caused by interactions of genetic, environmental, and other factors. Bile acid metabolism, as a key link between gut microbiota and the host, has been increasingly associated with the onset and development of PCOS. However, no systematic summary of this relationship is available so far. This review first discusses potential factors leading to bile acid pool changes in PCOS patients, including sex hormones, diet, and certain bacterial genera, which may promote PCOS by regulating bile acid metabolism. Bile acid signaling critically regulates host glucose and lipid homeostasis, follicular development, and sex hormone synthesis in a tissue-specific manner, indicating the limitations of focusing only on a single organ or cell type. Clinical studies show that bile acid metabolic profiles can distinguish PCOS patients from healthy controls, although the profiles are not fully consistent. Their heterogeneity is related to metabolic phenotypes, suggesting that bile acid profiling may help subtype PCOS. Given its role in insulin resistance, ovarian function, and steroid hormone synthesis, bile acid metabolism may act as a core hub in PCOS pathogenesis. Further mechanistic research is needed to better understand these processes and support the development of precise diagnostics and targeted therapies for PCOS.
Authors
- Wanzhen Li (ORCID: https://orcid.org/0000-0002-9980-7933)
- Xinyi Wu (ORCID: https://orcid.org/0000-0003-2365-6574)
- Min Wang (ORCID: https://orcid.org/0000-0002-3420-4031)
- Bingqi Wang
Institutions
- Central South University (CN)
- Second Xiangya Hospital of Central South University (CN)
Publication Details
- Journal
- Journal of Endocrinology
- Published
- 2026-04-24
- DOI
- https://doi.org/10.1530/joe-25-0225
- Primary Topic
- Ovarian function and disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00