| First Author | Smith EP | Year | 2014 |
| Journal | Cell Metab | Volume | 19 |
| Issue | 6 | Pages | 1050-7 |
| PubMed ID | 24836562 | Mgi Jnum | J:215246 |
| Mgi Id | MGI:5604953 | Doi | 10.1016/j.cmet.2014.04.005 |
| Citation | Smith EP, et al. (2014) The role of beta cell glucagon-like peptide-1 signaling in glucose regulation and response to diabetes drugs. Cell Metab 19(6):1050-7 |
| abstractText | Glucagon-like peptide-1 (GLP-1), an insulinotropic gut peptide released after eating, is essential for normal glucose tolerance (GT). To determine whether this effect is mediated directly by GLP-1 receptors (GLP1R) on islet beta cells, we developed mice with beta cell-specific knockdown of Glp1r. beta cell Glp1r knockdown mice had impaired GT after intraperitoneal (i.p.) glucose and did not secrete insulin in response to i.p. or intravenous GLP-1. However, they had normal GT after oral glucose, a response that was impaired by a GLP1R antagonist. beta cell Glp1r knockdown mice had blunted responses to a GLP1R agonist but intact glucose lowering with a dipeptidylpeptidase 4 (DPP-4) inhibitor. Thus, in mice, beta cell Glp1rs are required to respond to hyperglycemia and exogenous GLP-1, but other factors compensate for reduced GLP-1 action during meals. These results support a role for extraislet GLP1R in oral glucose tolerance and paracrine regulation of beta cells by islet GLP-1. |
