| First Author | Wang Q | Year | 2023 |
| Journal | Gut Microbes | Volume | 15 |
| Issue | 2 | Pages | 2274124 |
| PubMed ID | 37942583 | Mgi Jnum | J:355064 |
| Mgi Id | MGI:7640335 | Doi | 10.1080/19490976.2023.2274124 |
| Citation | Wang Q, et al. (2023) Gut microbiota regulates postprandial GLP-1 response via ileal bile acid-TGR5 signaling. Gut Microbes 15(2):2274124 |
| abstractText | The gut microbiota interacts with intestinal epithelial cells through microbial metabolites to regulate the release of gut hormones. We investigated whether the gut microbiota affects the postprandial glucagon-like peptide-1 (GLP-1) response using antibiotic-treated mice and germ-free mice. Gut microbiome depletion completely abolished postprandial GLP-1 response in the circulation and ileum in a lipid tolerance test. Microbiome depletion did not influence the GLP-1 secretory function of primary ileal cells in response to stimulators in vitro, but dramatically changed the postprandial dynamics of endogenous bile acids, particularly omega-muricholic acid (omegaMCA) and hyocholic acid (HCA). The bile acid receptor Takeda G protein-coupled receptor 5 (TGR5) but not farnesoid X receptor (FXR), participated in the regulation of postprandial GLP-1 response in the circulation and ileum, and omegaMCA or HCA stimulated GLP-1 secretion via TGR5. Finally, fecal microbiota transplantation or omegaMCA and HCA supplementation restored postprandial GLP-1 response. In conclusion, gut microbiota is indispensable for maintaining the postprandial GLP-1 response specifically in the ileum, and bile acid (omegaMCA and HCA)-TGR5 signaling is involved in this process. This study helps to understand the essential interplay between the gut microbiota and host in regulating postprandial GLP-1 response and opens the foundation for new therapeutic targets. |
