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Dietary and genetic control of glucose transporter 2 glycosylation promotes insulin secretion in suppressing diabetes.


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.

Pubmed ID: 16377570


  • Ohtsubo K
  • Takamatsu S
  • Minowa MT
  • Yoshida A
  • Takeuchi M
  • Marth JD



Publication Data

December 29, 2005

Associated Grants

  • Agency: NIDDK NIH HHS, Id: DK48247
  • Agency: NIGMS NIH HHS, Id: GM62116

Mesh Terms

  • Animals
  • Cells, Cultured
  • Diabetes Mellitus, Type 2
  • Diet
  • Dietary Fats
  • Glucose Transporter Type 2
  • Glycosylation
  • Insulin
  • Insulin-Secreting Cells
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • N-Acetylglucosaminyltransferases
  • Up-Regulation