Titre
Impact of Sur1 gene inactivation on the morphology of mouse pancreatic endocrine tissue.
Type
article
Institution
Externe
Périodique
Auteur(s)
Marhfour, I.
Auteure/Auteur
Moulin, P.
Auteure/Auteur
Marchandise, J.
Auteure/Auteur
Rahier, J.
Auteure/Auteur
Sempoux, C.
Auteure/Auteur
Guiot, Y.
Auteure/Auteur
Liens vers les personnes
ISSN
1432-0878
Statut éditorial
Publié
Date de publication
2009
Volume
335
Numéro
3
Première page
505
Dernière page/numéro d’article
515
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: ppublish
Résumé
In congenital hyperinsulinism of infancy (CHI), the loss of K-ATP channels (composed of Kir6.2 and SUR1 subunits) in beta cells induces permanent insulin secretion and severe hypoglycaemia. By contrast, Sur1 ( -/- ) mice do not present such defects. We have investigated the impact of Sur1 gene inactivation on mouse islet cell morphology, structure and basic physiology. Pancreata were collected from young, adult and old wild-type (WT) and Sur1 ( -/- ) mice. After immunostaining for hormone, the total endocrine tissue, cell proportion, cell size and intra-insular distribution, hormone content and Glut-2 expression were quantified by morphometry. Basic physiological parameters were also measured. In young Sur1 ( -/- ) mice, the total endocrine tissue and proportion of beta cells were higher (P<0.05) than in WT mice, whereas the proportion of delta cells was lower (P<0.01). In old Sur1 ( -/- ) mice, alpha cells were frequently located in the central regions of islets (unlike WT islets) and their proportion was increased (P<0.05). Glut-2 protein and mRNA levels were lower in old Sur1 ( -/- ) islets (P<0.02). Insulinaemia, fasting insulin and glucagon contents were equivalent in both groups of pancreata. Thus, the islets of Sur1 ( -/- ) mice present morphological modifications that have not been described in CHI and that might reflect an adaptive mechanism controlling insulin secretion in these mice.
Sujets
PID Serval
serval:BIB_1A614D2FB163
PMID
Date de création
2015-01-19T10:28:43.476Z
Date de création dans IRIS
2025-05-20T17:18:43Z