Gut microbiota and intestinal FXR mediate the clinical benefits of metformin
Open accessAbstract
The anti-hyperglycemic effect of metformin is believed to be caused by its direct action on signaling processes in hepatocytes, leading to lower hepatic gluconeogenesis. Recently, metformin was reported to alter the gut microbiota community in humans, suggesting that the hyperglycemia-lowering action of the drug could be the result of modulating the population of gut microbiota. However, the critical microbial signaling metabolites and the host targets associated with the metabolic benefits of metformin remained elusive. Here, we performed metagenomic and metabolomic analysis of samples from individuals with newly diagnosed type 2 diabetes (T2D) naively treated with metformin for 3 d, which revealed that Bacteroides fragilis was decreased and the bile acid glycoursodeoxycholic acid (GUDCA) was increased in the gut. These changes were accompanied by inhibition of intestinal farnesoid X receptor (FXR) signaling. We further found that high-fat-diet (HFD)-fed mice colonized with B. fragilis were predisposed to more severe glucose intolerance, and the metabolic benefits of metformin treatment on glucose intolerance were abrogated. GUDCA was further identified as an intestinal FXR antagonist that improved various metabolic endpoints in mice with established obesity. Thus, we conclude that metformin acts in part through a B. fragilis-GUDCA-intestinal FXR axis to improve metabolic dysfunction, including hyperglycemia.
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BA transformation by BSH-competent bacteria determines the magnitude of BA-induced nuclear FXR activation in the gut.
“BA transformation by BSH-competent bacteria determines the magnitude of BA-induced nuclear FXR activation in the gut (Long et al., 2017; Sun et al., 2018).”
From Bacteroides dorei BDX-01 alleviates DSS-induced experimental colitis in mice by regulating intestinal bile salt hydrolase activity and the FXR-NLRP3 signaling pathway (2023) · cites this paper as Sun et al., 2018
Metformin improves metabolic dysfunction in diabetics by increasing bile acid GUDCA through inhibiting growth of B. fragilis, altering intestinal FXR signaling.
“metformin’s role in improving metabolic dysfunction in diabetics was linked to an increase in levels of bile acid glycoursodeoxycholic acid (GUDCA) by inhibiting the growth of B. fragilis, thereby altering intestinal Farnesoid X Receptor (FXR) signaling”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as Sun et al. 2018
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- Authors
- Sun, L., Xie, C., Wang, G., Wu, Y., Wu, Q., Wang, X., Liu, J., Deng, Y., Xia, J., Chen, B., Zhang, S., Yun, C., Lian, G., Zhang, X., Zhang, H., Bisson, W. H., Shi, J., Gao, X., Ge, P., Liu, C., Krausz, K. W., Nichols, R. G., Cai, J., Rimal, B., Patterson, A. D., Wang, X., Gonzalez, F. J., & Jiang, C.
- Affiliations
- Peking University (CN)
- National Institutes of Health (US)
- Capital Medical University (CN)
- First Affiliated Hospital of Xi'an Jiaotong University (CN)
- Oregon State University (US)
- Chinese Academy of Sciences (CN)
- Pennsylvania State University (US)
- Corresponding author
- Jiang, Changtao
- ORCID
- Venue
- Nature Medicine
- Published
- 2018-11-05
- Volume
- 24
- Issue
- 12
- Pages
- 1919-1929
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC6479226
- OpenAlex
- W2898587007
- Cited by
- 1,011
- References
- 49
- Citations by year
- 2026: 107 · 2025: 126 · 2024: 174 · 2023: 153 · 2022: 141 · 2021: 130 · 2020: 102 · 2019: 71 · 2018: 6
- FWCI
- 27.47
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (Z01BC005561)
- National Institute of General Medical Sciences (T32GM102057)
- U.S. National Library of Medicine (T32LM012415)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Keywords
- metformin, gut microbiota, Bacteroides fragilis, glycoursodeoxycholic acid, bile acids, type 2 diabetes, impaired glucose tolerance, obesity, hyperglycemia, high-fat diet, hepatic gluconeogenesis, microbial metabolites
- MeSH terms
- Gastrointestinal Microbiome, Receptor, Farnesoid X-Activated, Bacteroides, Bile Acids and Salts, Diabetes Mellitus, Type 2, Humans, Hyperglycemia, Metformin, Obesity, Ursodeoxycholic Acid, Gene Expression Regulation, Bacterial, Glucose Intolerance, Receptors, Cytoplasmic and Nuclear, Metabolome, Metagenomics, Diet, High-Fat
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