Diabetic hyperglyeemia

Link to impaired glucose transport in pancreatic β cells

Research output: Contribution to journalArticle

237 Citations (Scopus)

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 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
StatePublished - Mar 8 1991

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Type 1 Diabetes Mellitus
Glucose
Hyperglycemia
Facilitative Glucose Transport Proteins
Immunoglobulins
Down-Regulation
Insulin

ASJC Scopus subject areas

  • General

Cite this

Diabetic hyperglyeemia : Link to impaired glucose transport in pancreatic β cells. / Unger, Roger H.

In: Science, Vol. 251, No. 4998, 08.03.1991, p. 1200-1205.

Research output: Contribution to journalArticle

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