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ludc web

Anna Wendt

Assistant researcher

ludc web

Intra-islet insulin suppresses glucagon release via GABA-GABA(A) receptor system

Author

  • E Xu
  • M Kumar
  • Y Zhang
  • W Ju
  • T Obata
  • N Zhang
  • SY Liu
  • Anna Wendt
  • SP Deng
  • Y Ebina
  • MB Wheeler
  • Matthias Braun
  • QH Wang

Summary, in English

Excessive secretion of glucagon is a major contributor to the development of diabetic hyperglycemia. Secretion of glucagon is regulated by various nutrients, with glucose being a primary determinant of the rate of alpha cell glucagon secretion. The intra-islet action of insulin is essential to exert the effect of glucose on the alpha cells since, in the absence of insulin, glucose is not able to suppress glucagon release in vivo. However, the precise mechanism by which insulin suppresses glucagon secretion from a cells is unknown. In this study, we show that insulin induces activation of GABA(A) receptors in the alpha cells by receptor translocation via an Akt kinase-dependent pathway. This leads to membrane hyperpolarization in the alpha cells and, ultimately, suppression of glucagon secretion. We propose that defects in this pathway(s) contribute to diabetic hyperglycemia.

Department/s

  • Diabetes - Islet Cell Exocytosis
  • Islet cell physiology

Publishing year

2006

Language

English

Pages

47-58

Publication/Series

Cell Metabolism

Volume

3

Issue

1

Document type

Journal article

Publisher

Cell Press

Topic

  • Cell and Molecular Biology

Status

Published

Research group

  • Diabetes - Islet Cell Exocytosis
  • Islet cell physiology

ISBN/ISSN/Other

  • ISSN: 1550-4131