Incretin receptor null mice reveal key role of GLP-1 but not GIP in pancreatic beta cell adaptation to pregnancy.

Détails

Ressource 1Télécharger: BIB_3C41D2B7D38E.P001.pdf (3283.19 [Ko])
Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_3C41D2B7D38E
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Incretin receptor null mice reveal key role of GLP-1 but not GIP in pancreatic beta cell adaptation to pregnancy.
Périodique
PLoS One
Auteur(s)
Moffett R.C., Vasu S., Thorens B., Drucker D.J., Flatt P.R.
ISSN
1932-6203 (Electronic)
ISSN-L
1932-6203
Statut éditorial
Publié
Date de publication
2014
Volume
9
Numéro
6
Pages
e96863
Langue
anglais
Résumé
Islet adaptations to pregnancy were explored in C57BL6/J mice lacking functional receptors for glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP). Pregnant wild type mice and GIPRKO mice exhibited marked increases in islet and beta cell area, numbers of medium/large sized islets, with positive effects on Ki67/Tunel ratio favouring beta cell growth and enhanced pancreatic insulin content. Alpha cell area and glucagon content were unchanged but prohormone convertases PC2 and PC1/3 together with significant amounts of GLP-1 and GIP were detected in alpha cells. Knockout of GLP-1R abolished these islet adaptations and paradoxically decreased pancreatic insulin, GLP-1 and GIP. This was associated with abolition of normal pregnancy-induced increases in plasma GIP, L-cell numbers, and intestinal GIP and GLP-1 stores. These data indicate that GLP-1 but not GIP is a key mediator of beta cell mass expansion and related adaptations in pregnancy, triggered in part by generation of intra-islet GLP-1.
Pubmed
Web of science
Open Access
Oui
Création de la notice
08/08/2014 19:39
Dernière modification de la notice
20/08/2019 13:32
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