Agmatine produced by gut microbiota — specifically, Bacteroides vulgatus — activates the farnesoid X receptor (FXR) in intestinal epithelial L cells in a bile-acid-independent manner, which inhibits host glucagon peptide 1 (GLP-1) secretion and leads to polycystic ovary syndrome (PCOS) in mice. Supplementing mice with the GLP-1 receptor (GLP-1R) agonist liraglutide or inhibiting the production of agmatine reverses the PCOS phenotype.
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References
Qi, X. et al. Gut microbiota-bile acid-interleukin-22 axis orchestrates polycystic ovary syndrome. Nat. Med. 25, 1225–1233 (2019). This paper reports on the mechanism of how B. vulgatus induces PCOS through the bile-acid–IL-22 pathway.
Trabelsi, M.-S. et al. Farnesoid X receptor inhibits glucagon-like peptide-1 production by enteroendocrine L cells. Nat. Commun. 6, 7629 (2015). This paper reports on the FXR–GLP-1 pathway in enteroendocrine L cells.
Jensterle, M. et al. The role of glucagon-like peptide-1 in reproduction: from physiology to therapeutic perspective. Hum. Reprod. Update 25, 504–517 (2019). A review that presents the potential role of GLP-1 in the pathogenesis and treatment of PCOS.
Drucker, D. J. Mechanisms of action and therapeutic application of glucagon-like peptide-1. Cell Metab. 27, 740–756 (2018). A review that presents the mechanisms of action, side effects and applications of existing GLP-1R agonists.
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This is a summary of: Yun, C. et al. The microbial metabolite agmatine acts as an FXR agonist to promote polycystic ovary syndrome in female mice. Nat. Metab. https://doi.org/10.1038/s42255-024-01041-8 (2024).
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The microbial metabolite agmatine induces polycystic ovary syndrome in mice. Nat Metab 6, 791–792 (2024). https://doi.org/10.1038/s42255-024-01040-9
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DOI: https://doi.org/10.1038/s42255-024-01040-9
