Diabetic hyperglycemia: Link to impaired glucose transport in pancreatic β cells

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246 Scopus citations

Abstract

Glucose uptake into pancreatic β cells by means of the glucose transporter GLUT-2, which has a high Michaelis constant, is essential for the normal insulin secretory response to hyperglycemia. In both autoimmune and nonautoimmune diabetes, this glucose transport is reduced as a consequence of down-regulation of the normal β-cell transporter. In autoimmune diabetes, circulating immunoglobulins can further impair this glucose transport by inhibiting functionally intact transporters. Insights into mechanisms of the unresponsiveness of β cells to hyperglycemia may improve the management and prevention of diabetes.

Original languageEnglish (US)
Pages (from-to)1200-1205
Number of pages6
JournalScience
Volume251
Issue number4998
DOIs
StatePublished - Jan 1 1991

ASJC Scopus subject areas

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