Involvement of the Adhesion GPCRs Latrophilins in the Regulation of Insulin Release.
adhesion GPCRs
insulin secretion
latrophilins
signaling
splice variants
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
05 02 2019
05 02 2019
Historique:
received:
04
10
2018
revised:
21
12
2018
accepted:
10
01
2019
entrez:
7
2
2019
pubmed:
7
2
2019
medline:
9
4
2020
Statut:
ppublish
Résumé
Insulin secretion from pancreatic β cells is a highly complex and tightly regulated process. Its dysregulation is one characteristic of type 2 diabetes, and thus, an in-depth understanding of the mechanisms controlling insulin secretion is essential for rational therapeutic intervention. G-protein-coupled receptors (GPCRs) have been established as major regulators of insulin exocytosis. Recent studies also suggest the involvement of adhesion GPCRs, a non-prototypical class of GPCRs. Here, we identify latrophilins, which belong to the class of adhesion GPCRs, to be highly expressed in different cell types of pancreatic islets. In vitro and ex vivo analyses show that distinct splice variants of the latrophilin LPHN3/ADGRL3 decrease insulin secretion from pancreatic β cells by reducing intracellular cyclic AMP levels via the G
Identifiants
pubmed: 30726739
pii: S2211-1247(19)30058-0
doi: 10.1016/j.celrep.2019.01.040
pii:
doi:
Substances chimiques
LPHN3 protein, mouse
0
Receptors, G-Protein-Coupled
0
Receptors, Peptide
0
Cyclic AMP
E0399OZS9N
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1573-1584.e5Informations de copyright
Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.