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

Ying YunShimeng GuoXin Xie
Published in: Cell & bioscience (2024)
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.
Keyphrases
  • induced apoptosis
  • blood glucose
  • cell cycle arrest
  • cancer therapy
  • signaling pathway
  • cell death
  • drug delivery
  • adipose tissue
  • metabolic syndrome
  • insulin resistance
  • skeletal muscle