| First Author | Wang L | Year | 2019 |
| Journal | Biochem Biophys Res Commun | Volume | 510 |
| Issue | 1 | Pages | 104-109 |
| PubMed ID | 30661789 | Mgi Jnum | J:290267 |
| Mgi Id | MGI:6442098 | Doi | 10.1016/j.bbrc.2019.01.055 |
| Citation | Wang L, et al. (2019) Toll-like receptor 4 is necessary for glucose-dependent glucagon-like peptide-1 secretion in male mice. Biochem Biophys Res Commun 510(1):104-109 |
| abstractText | Lipopolysaccharide (LPS), a natural toll-like receptor 4 (TLR4) ligand, can induce the secretion of glucagon-like peptide-1 (GLP-1) in both animal models and humans consistent with the notion that TLR4 may influence physiological process of GLP-1 secretion. Here, we explored the possible role of TLR4 in the process of glucose-dependent GLP-1 secretion. Wild-type and TLR4 knockout mice were used to observe GLP-1 expression and secretion, as well as the cytokines tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6) levels in plasma and ileum after glucose load. TLR4 deficient mice also were given an injection of TNF-alpha and IL-6, respectively, to confirm the key role of TLR4-mediated inflammatory cytokines in the process of glucose-induced GLP-1 secretion. We found that the TLR4 deficiency impaired the glucose-induced GLP-1 release and prevented an increase in IL-6 and TNF-alpha levels in plasma and ileum following glucose stimulation. Importantly, injection of TLR4 deficient mice with either TNF-alpha and IL-6 partly restored the glucose-induced secretion of GLP-1. In conclusion, the production of pro-inflammatory cytokines downstream of TLR4 promotes glucose-dependent GLP-1 secretion from intestinal L-cells in mice. |
