Underexpression of beta cell high Km glucose transporters in noninsulin-dependent diabetes.

Journal Article

The role of defective glucose transport in the pathogenesis of noninsulin-dependent diabetes (NIDDM) was examined in Zucker diabetic fatty rats, a model of NIDDM. As in human NIDDM, insulin secretion was unresponsive to 20 mM glucose. Uptake of 3-O-methylglucose by islet cells was less than 19% of controls. The beta cell glucose transporter (GLUT-2) immunoreactivity and amount of GLUT-2 messenger RNA were profoundly reduced. Whenever fewer than 60% of beta cells were GLUT-2-positive, the response to glucose was absent and hyperglycemia exceeded 11 mM plasma glucose. We conclude that in NIDDM underexpression of GLUT-2 messenger RNA lowers high Km glucose transport in beta cells, and thereby impairs glucose-stimulated insulin secretion and prevents correction of hyperglycemia.

Full Text

Duke Authors

Cited Authors

  • Johnson, JH; Ogawa, A; Chen, L; Orci, L; Newgard, CB; Alam, T; Unger, RH

Published Date

  • October 26, 1990

Published In

Volume / Issue

  • 250 / 4980

Start / End Page

  • 546 - 549

PubMed ID

  • 2237405

International Standard Serial Number (ISSN)

  • 0036-8075

Language

  • eng

Conference Location

  • United States