TY - JOUR T1 - TRPV1 Mediates Glucose-induced Insulin Secretion Through Releasing Neuropeptides JF - In Vivo JO - In Vivo SP - 1431 LP - 1437 DO - 10.21873/invivo.11621 VL - 33 IS - 5 AU - BEIHUA ZHONG AU - SHUANGTAO MA AU - DONNA H. WANG Y1 - 2019/09/01 UR - http://iv.iiarjournals.org/content/33/5/1431.abstract N2 - 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. ER -