Beta-cell M
Acetylcholine
Allosteric modulator
Beta-cell
Diabetes
G protein-coupled receptor
Insulin release
Muscarinic receptor
Journal
International immunopharmacology
ISSN: 1878-1705
Titre abrégé: Int Immunopharmacol
Pays: Netherlands
ID NLM: 100965259
Informations de publication
Date de publication:
Apr 2020
Apr 2020
Historique:
received:
29
11
2019
revised:
25
01
2020
accepted:
27
01
2020
pubmed:
12
2
2020
medline:
8
1
2021
entrez:
12
2
2020
Statut:
ppublish
Résumé
A key feature of type 2 diabetes (T2D) is that beta-cells of the pancreatic islets fail to release sufficient amounts of insulin to overcome peripheral insulin resistance. Glucose-stimulated insulin secretion (GSIS) is regulated by the activity of numerous neurotransmitters, hormones and paracrine factors that act by stimulating specific G protein-coupled receptors expressed by pancreatic beta-cells. Studies with both mouse and human islets suggest that acetylcholine (ACh) acts on beta-cell M
Identifiants
pubmed: 32044662
pii: S1567-5769(19)32779-1
doi: 10.1016/j.intimp.2020.106267
pii:
doi:
Substances chimiques
Insulin
0
Receptor, Muscarinic M3
0
Receptors, Cholinergic
0
Acetylcholine
N9YNS0M02X
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
106267Informations de copyright
Published by Elsevier B.V.
Déclaration de conflit d'intérêts
Declaration of Competing Interest None of the authors has any conflicts of interest regarding this submission.