14-3-3-zeta mediates GLP-1 receptor agonist action to alter α cell proglucagon processing.
Journal
Science advances
ISSN: 2375-2548
Titre abrégé: Sci Adv
Pays: United States
ID NLM: 101653440
Informations de publication
Date de publication:
22 Jul 2022
22 Jul 2022
Historique:
entrez:
22
7
2022
pubmed:
23
7
2022
medline:
23
7
2022
Statut:
ppublish
Résumé
Recent studies demonstrate that α cells contribute to glucose-stimulated insulin secretion (GSIS). Glucagon-like peptide-1 receptor (GLP-1R) agonists potently potentiate GSIS, making these drugs useful for diabetes treatment. However, the role of α and β cell paracrine interactions in the effects of GLP-1R agonists is undefined. We previously found that increased β cell GLP-1R signaling activates α cell GLP-1 expression. Here, we characterized the bidirectional paracrine cross-talk by which α and β cells communicate to mediate the effects of the GLP-1R agonist, liraglutide. We find that the effect of liraglutide to enhance GSIS is blunted by α cell ablation in male mice. Furthermore, the effect of β cell GLP-1R signaling to activate α cell GLP-1 is mediated by a secreted protein factor that is regulated by the signaling protein, 14-3-3-zeta, in mouse and human islets. These data refine our understanding of GLP-1 pharmacology and identify 14-3-3-zeta as a potential target to enhance α cell GLP-1 production.
Identifiants
pubmed: 35867787
doi: 10.1126/sciadv.abn3773
pmc: PMC9307243
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
eabn3773Subventions
Organisme : NIDDK NIH HHS
ID : F30 DK126538
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK020541
Pays : United States
Organisme : NIH HHS
ID : T35 OD010941
Pays : United States
Organisme : NIDDK NIH HHS
ID : U24 DK098085
Pays : United States
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