| First Author | Zhong B | Year | 2019 |
| Journal | In Vivo | Volume | 33 |
| Issue | 5 | Pages | 1431-1437 |
| PubMed ID | 31471389 | Mgi Jnum | J:290777 |
| Mgi Id | MGI:6435463 | Doi | 10.21873/invivo.11621 |
| Citation | Zhong B, et al. (2019) TRPV1 Mediates Glucose-induced Insulin Secretion Through Releasing Neuropeptides. In Vivo 33(5):1431-1437 |
| abstractText | BACKGROUND/AIM: Transient receptor potential vanilloid 1 (TRPV1)-expressing sensory nerves innervate the pancreatic islets. Sensory neuropeptides, including calcitonin gene-related peptide (CGRP) and substance P (SP), participate in insulin secretion. This study aimed to investigate the role of TRPV1 in glucose-induced insulin secretion. MATERIALS AND METHODS: TRPV1(-/-) and wild-type (WT) mice were fed a normal diet for 24 weeks. Glucose tolerance and insulin secretion were measured at the end of the experiments. RESULTS: TRPV1(-/-) mice had greater impairments in glucose tolerance and higher decrease in glucose-induced insulin secretion than WT mice. Capsaicin (a TRPV1 agonist) increased insulin secretion in WT, but not in TRPV1(-/-) mice. Glucose-induced insulin secretion was blunted in TRPV1(-/-) mice, and was attenuated by AMG9810 (a TRPV1 inhibitor), CGRP8-37 (a CGRP receptor antagonist), or RP67580 (a NK-1 receptor antagonist) in WT mice. Glucose-induced SP and CGRP release from WT pancreas was higher than that from TRPV1(-/-) pancreas. CONCLUSION: TRPV1 mediates glucose-induced insulin secretion likely through CGRP and SP release. |
