Islet G protein-coupled receptors as potential targets for treatment of type 2 diabetes.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1392126
- author
- Ahrén, Bo LU
- organization
- publishing date
- 2009
- 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
- 2016-04-01 12:12:25
- date last changed
- 2024-01-23 10:00:04
@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}},
doi = {{10.1038/nrd2782}},
volume = {{8}},
year = {{2009}},
}