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Islet G protein-coupled receptors as potential targets for treatment of type 2 diabetes.

Ahrén, Bo LU (2009) In Nature Reviews. Drug Discovery 8(5). p.369-385
Abstract
Islet dysfunction - characterized by a combination of defective insulin secretion, inappropriately high glucagon secretion and reduced beta-cell mass - has a central role in the pathophysiology of type 2 diabetes. Several G protein-coupled receptors (GPCRs) expressed in islet beta-cells are known to be involved in the regulation of islet function, and therefore are potential therapeutic targets. This is evident from the recent success of glucagon-like peptide 1 (GLP1) mimetics and dipeptidyl peptidase 4 (DPP4) inhibitors, which promote activation of the GLP1 receptor to stimulate insulin secretion and inhibit glucagon secretion, and also have the potential to increase beta-cell mass. Other islet beta-cell GPCRs that are involved in the... (More)
Islet dysfunction - characterized by a combination of defective insulin secretion, inappropriately high glucagon secretion and reduced beta-cell mass - has a central role in the pathophysiology of type 2 diabetes. Several G protein-coupled receptors (GPCRs) expressed in islet beta-cells are known to be involved in the regulation of islet function, and therefore are potential therapeutic targets. This is evident from the recent success of glucagon-like peptide 1 (GLP1) mimetics and dipeptidyl peptidase 4 (DPP4) inhibitors, which promote activation of the GLP1 receptor to stimulate insulin secretion and inhibit glucagon secretion, and also have the potential to increase beta-cell mass. Other islet beta-cell GPCRs that are involved in the regulation of islet function include the glucose-dependent insulinotropic peptide (GIP) receptor, lipid GPCRs, pleiotropic peptide GPCRs and islet biogenic amine GPCRs. This Review summarizes islet GPCR expression, signalling and function, and highlights their potential as targets for the treatment of type 2 diabetes. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Nature Reviews. Drug Discovery
volume
8
issue
5
pages
369 - 385
publisher
Nature Publishing Group
external identifiers
  • wos:000265587500019
  • pmid:19365392
  • scopus:67349176115
ISSN
1474-1776
DOI
10.1038/nrd2782
language
English
LU publication?
yes
id
da44dede-b143-45d9-bc8f-21e21d447901 (old id 1392126)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/19365392?dopt=Abstract
date added to LUP
2009-05-06 13:41:49
date last changed
2017-12-10 03:49:29
@article{da44dede-b143-45d9-bc8f-21e21d447901,
  abstract     = {Islet dysfunction - characterized by a combination of defective insulin secretion, inappropriately high glucagon secretion and reduced beta-cell mass - has a central role in the pathophysiology of type 2 diabetes. Several G protein-coupled receptors (GPCRs) expressed in islet beta-cells are known to be involved in the regulation of islet function, and therefore are potential therapeutic targets. This is evident from the recent success of glucagon-like peptide 1 (GLP1) mimetics and dipeptidyl peptidase 4 (DPP4) inhibitors, which promote activation of the GLP1 receptor to stimulate insulin secretion and inhibit glucagon secretion, and also have the potential to increase beta-cell mass. Other islet beta-cell GPCRs that are involved in the regulation of islet function include the glucose-dependent insulinotropic peptide (GIP) receptor, lipid GPCRs, pleiotropic peptide GPCRs and islet biogenic amine GPCRs. This Review summarizes islet GPCR expression, signalling and function, and highlights their potential as targets for the treatment of type 2 diabetes.},
  author       = {Ahrén, Bo},
  issn         = {1474-1776},
  language     = {eng},
  number       = {5},
  pages        = {369--385},
  publisher    = {Nature Publishing Group},
  series       = {Nature Reviews. Drug Discovery},
  title        = {Islet G protein-coupled receptors as potential targets for treatment of type 2 diabetes.},
  url          = {http://dx.doi.org/10.1038/nrd2782},
  volume       = {8},
  year         = {2009},
}