V1bR enhances glucose-stimulated insulin secretion by paracrine production of glucagon which activates GLP-1 receptor.

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-depe

SUBMITTER: Yun Y 

PROVIDER: S-EPMC11365140 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature