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

Fiche du document

Date

2012

Type de document
Périmètre
Langue
Identifiants
Relations

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/doi/10.1172/JCI64151

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/pmid/22996663

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/eissn/1558-8238

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_3EFD603B48DE5

Licences

info:eu-repo/semantics/openAccess , Copying allowed only for non-profit organizations , https://serval.unil.ch/disclaimer



Citer ce document

C. Jacovetti et al., « MicroRNAs contribute to compensatory β cell expansion during pregnancy and obesity. », Serveur académique Lausannois, ID : 10.1172/JCI64151


Métriques


Partage / Export

Résumé 0

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.

document thumbnail

Par les mêmes auteurs

Sur les mêmes sujets

Exporter en