MicroRNAs contribute to compensatory β cell expansion during pregnancy and obesity.

Détails

Ressource 1Télécharger: Jacovetti JCI 2012 (5).pdf (1172.52 [Ko])
Etat: Public
Version: Final published version
ID Serval
serval:BIB_3EFD603B48DE
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
MicroRNAs contribute to compensatory β cell expansion during pregnancy and obesity.
Périodique
Journal of Clinical Investigation
Auteur(s)
Jacovetti C., Abderrahmani A., Parnaud G., Jonas J.C., Peyot M.L., Cornu M., Laybutt R., Meugnier E., Rome S., Thorens B., Prentki M., Bosco D., Regazzi R.
ISSN
1558-8238 (Electronic)
ISSN-L
0021-9738
Statut éditorial
Publié
Date de publication
2012
Peer-reviewed
Oui
Volume
122
Numéro
10
Pages
3541-3551
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: ppublish
Résumé
Pregnancy and obesity are frequently associated with diminished insulin sensitivity, which is normally compensated for by an expansion of the functional β cell mass that prevents chronic hyperglycemia and development of diabetes mellitus. The molecular basis underlying compensatory β cell mass expansion is largely unknown. We found in rodents that β cell mass expansion during pregnancy and obesity is associated with changes in the expression of several islet microRNAs, including miR-338-3p. In isolated pancreatic islets, we recapitulated the decreased miR-338-3p level observed in gestation and obesity by activating the G protein-coupled estrogen receptor GPR30 and the glucagon-like peptide 1 (GLP1) receptor. Blockade of miR-338-3p in β cells using specific anti-miR molecules mimicked gene expression changes occurring during β cell mass expansion and resulted in increased proliferation and improved survival both in vitro and in vivo. These findings point to a major role for miR-338-3p in compensatory β cell mass expansion occurring under different insulin resistance states.
Pubmed
Web of science
Open Access
Oui
Création de la notice
31/10/2012 13:59
Dernière modification de la notice
20/08/2019 13:35
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