Dataset Information
V1bR enhances glucose-stimulated insulin secretion by paracrine production of glucagon which activates GLP-1 receptor.
Ontology highlight
ABSTRACT: Background
Arginine vasopressin (AVP) has been reported to regulate insulin secretion and glucose homeostasis in the body. Previous study has shown that AVP and its receptor V1bR modulate insulin secretion via the hypothalamic-pituitary-adrenal axis. AVP has also been shown to enhance insulin secretion in islets, but the exact mechanism remains unclear.Results
In our study, we unexpectedly discovered that AVP could only stimulates insulin secretion from islets, but not β cells, and AVP-induced insulin secretion could be blocked by V1bR selective antagonist. Single-cell transcriptome analysis identified that V1bR is only expressed by the α cells. Further studies indicated that activation of the V1bR stimulates the α cells to secrete glucagon, which then promotes glucose-dependent insulin secretion from β cells in a paracrine way by activating GLP-1R but not GCGR on these cells.Conclusions
Our study revealed a crosstalk between α and β cells initiated by AVP/V1bR and mediated by glucagon/GLP-1R, providing a mechanism to develop new glucose-controlling therapies targeting V1bR.
SUBMITTER: Yun Y
PROVIDER: S-EPMC11365140 | biostudies-literature | 2024 Aug
REPOSITORIES: biostudies-literature
Publications
V1bR enhances glucose-stimulated insulin secretion by paracrine production of glucagon which activates GLP-1 receptor.
Cell & bioscience 20240831 1
<h4>Background</h4>Arginine vasopressin (AVP) has been reported to regulate insulin secretion and glucose homeostasis in the body. Previous study has shown that AVP and its receptor V1bR modulate insulin secretion via the hypothalamic-pituitary-adrenal axis. AVP has also been shown to enhance insulin secretion in islets, but the exact mechanism remains unclear.<h4>Results</h4>In our study, we unexpectedly discovered that AVP could only stimulates insulin secretion from islets, but not β cells, a ...[more]