The DOI matches its Crossref record; 27 of the 27 references it cites were found in a registry or an index.
Gut microbiota–bile acid–interleukin-22 axis orchestrates polycystic ovary syndrome
Open accessAbstract
Polycystic ovary syndrome (PCOS) is characterized by androgen excess, ovulatory dysfunction and polycystic ovaries1, and is often accompanied by insulin resistance2. The mechanism of ovulatory dysfunction and insulin resistance in PCOS remains elusive, thus limiting the development of therapeutics. Improved metabolic health is associated with a relatively high microbiota gene content and increased microbial diversity3,4. This study aimed to investigate the impact of the gut microbiota and its metabolites on the regulation of PCOS-associated ovarian dysfunction and insulin resistance. Here, we report that Bacteroides vulgatus was markedly elevated in the gut microbiota of individuals with PCOS, accompanied by reduced glycodeoxycholic acid and tauroursodeoxycholic acid levels. Transplantation of fecal microbiota from women with PCOS or B. vulgatus-colonized recipient mice resulted in increased disruption of ovarian functions, insulin resistance, altered bile acid metabolism, reduced interleukin-22 secretion and infertility. Mechanistically, glycodeoxycholic acid induced intestinal group 3 innate lymphoid cell IL-22 secretion through GATA binding protein 3, and IL-22 in turn improved the PCOS phenotype. This finding is consistent with the reduced levels of IL-22 in individuals with PCOS. This study suggests that modifying the gut microbiota, altering bile acid metabolism and/or increasing IL-22 levels may be of value for the treatment of PCOS. Modifying the gut microbiota, bile acid, or IL-22 may offer an alternative approach for the treatment of polycystic ovary syndrome.
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Cited by
The impact of the gut microbiota on the reproductive and metabolic endocrine system
Qi, X., Yun, C., Pang, Y., & Qiao, J. (2021) · Gut Microbes · doi:10.1080/19490976.2021.1894070 · Cited by 554
Self-citationPolycystic Ovary Syndrome: Etiology, Current Management, and Future Therapeutics
Singh, S., Pal, N., Shubham, S., Sarma, D. K., Verma, V., Marotta, F., & Kumar, M. (2023) · Journal of Clinical Medicine · doi:10.3390/jcm12041454 · Cited by 521
Animal Models to Understand the Etiology and Pathophysiology of Polycystic Ovary Syndrome
Stener-Victorin, E., Padmanabhan, V., Walters, K. A., Campbell, R. E., Benrick, A., Giacobini, P., Dumesic, D. A., & Abbott, D. H. (2020) · Endocrine Reviews · doi:10.1210/endrev/bnaa010 · Cited by 348
Cong, J., Liu, P., Han, Z., Ying, W., Li, C., Yang, Y., Wang, S., Yang, J., Cao, F., Shen, J., et al. (2024) · Immunity · doi:10.1016/j.immuni.2024.02.014 · Cited by 303
Self-citationHe, F.-F., & Li, Y.-M. (2020) · Journal of Ovarian Research · doi:10.1186/s13048-020-00670-3 · Cited by 289
Metadata
- Authors
- Qi, X., Yun, C., Sun, L., Xia, J., Wu, Q., Wang, Y., Wang, L., Zhang, Y., Liang, X., Wang, L., Gonzalez, F. J., Patterson, A. D., Liu, H., Mu, L., Zhou, Z., Zhao, Y., Li, R., Liu, P., Zhong, C., Pang, Y., Jiang, C., & Qiao, J.
- Venue
- Nature Medicine
- Published
- 2019-07-22
- Volume
- 25
- Issue
- 8
- Pages
- 1225-1233
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2963985015
- Cited by
- 846
- References
- 27
- FWCI
- 56.72
- Type
- journal article
- Language
- en
- Open access
- green
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- Qi, X., Yun, C., Sun, L., Xia, J., Wu, Q., Wang, Y., Wang, L., Zhang, Y., Liang, X., Wang, L., Gonzalez, F. J., Patterson, A. D., Liu, H., Mu, L., Zhou, Z., Zhao, Y., Li, R., Liu, P., Zhong, C., . . . Qiao, J. (2019). Gut microbiota–bile acid–interleukin-22 axis orchestrates polycystic ovary syndrome. Nature Medicine. https://doi.org/10.1038/s41591-019-0509-0
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