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

Xu, E ; Kumar, M ; Zhang, Y ; Ju, W ; Obata, T ; Zhang, N ; Liu, SY ; Wendt, Anna LU ; Deng, SP and Ebina, Y , et al. (2006) In Cell Metabolism 3(1). p.47-58
Abstract
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... (More)
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. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Cell Metabolism
volume
3
issue
1
pages
47 - 58
publisher
Cell Press
external identifiers
  • wos:000234589300008
  • scopus:33645051453
ISSN
1550-4131
DOI
10.1016/j.cmet.2005.11.015
language
English
LU publication?
yes
id
d9dc56a2-be94-481f-99e3-9e79f0bb672c (old id 421397)
alternative location
http://www.cellmetabolism.org/content/article/abstract?uid=PIIS1550413105003748
date added to LUP
2016-04-01 12:37:43
date last changed
2021-10-03 05:16:39
@article{d9dc56a2-be94-481f-99e3-9e79f0bb672c,
  abstract     = {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.},
  author       = {Xu, E and Kumar, M and Zhang, Y and Ju, W and Obata, T and Zhang, N and Liu, SY and Wendt, Anna and Deng, SP and Ebina, Y and Wheeler, MB and Braun, Matthias and Wang, QH},
  issn         = {1550-4131},
  language     = {eng},
  number       = {1},
  pages        = {47--58},
  publisher    = {Cell Press},
  series       = {Cell Metabolism},
  title        = {Intra-islet insulin suppresses glucagon release via GABA-GABA(A) receptor system},
  url          = {http://dx.doi.org/10.1016/j.cmet.2005.11.015},
  doi          = {10.1016/j.cmet.2005.11.015},
  volume       = {3},
  year         = {2006},
}