References
Query Results -- Details
MGI Accession ID: MGI:3696712
J Number: J:117542
Other Accession IDs:
Title: Dietary and genetic control of glucose transporter 2 glycosylation promotes insulin secretion in suppressing diabetes.
Authors: Ohtsubo K; Takamatsu S; Minowa MT; Yoshida A; Takeuchi M; Marth JD
Journal: Cell
Volume: 123
Issue: 7
Date: 2005 Dec 29
Year: 2005
Pages: 1307-21
Review Status: Peer Reviewed
Abstract:
Pancreatic beta cell-surface expression of glucose transporter 2 (Glut-2) is essential for glucose-stimulated insulin secretion, thereby controlling blood glucose homeostasis in response to dietary intake. We show that the murine GlcNAcT-IVa glycosyltransferase is required for Glut-2 residency on the beta cell surface by constructing a cell-type- and glycoprotein-specific N-glycan ligand for pancreatic lectin receptors. Loss of GlcNAcT-IVa, or the addition of glycan-ligand mimetics, attenuates Glut-2 cell-surface half-life, provoking endocytosis with redistribution into endosomes and lysosomes. The ensuing impairment of glucose-stimulated insulin secretion leads to metabolic dysfunction diagnostic of type 2 diabetes. Remarkably, the induction of diabetes by chronic ingestion of a high-fat diet is associated with reduced GlcNAcT-IV expression and attenuated Glut-2 glycosylation coincident with Glut-2 endocytosis. We infer that beta cell glucose-transporter glycosylation mediates a link between diet and insulin production that typically suppresses the pathogenesis of type 2 diabetes.
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