A radical explanation for glucose-induced β cell dysfunction

Michael Brownlee

Research output: Contribution to journalArticle

174 Citations (Scopus)

Abstract

The development of type 2 diabetes requires impaired β cell function. Hyperglycemia itself causes further decreases in glucose-stimulated insulin secretion. A new study demonstrates that hyperglycemia-induced mitochondrial superoxide production activates uncoupling protein 2, which decreases the ATP/ADP ratio and thus reduces the insulin-secretory response (see the related article beginning on page 1831). These data suggest that pharmacologic inhibition of mitochondrial superoxide overproduction in β cells exposed to hyperglycemia could prevent a positive feed-forward loop of glucotoxicity that drives impaired glucose tolerance toward frank type 2 diabetes.

Original languageEnglish (US)
Pages (from-to)1788-1790
Number of pages3
JournalJournal of Clinical Investigation
Volume112
Issue number12
DOIs
StatePublished - Dec 2003

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Hyperglycemia
Glucose
Superoxides
Type 2 Diabetes Mellitus
Insulin
Glucose Intolerance
Adenosine Diphosphate
Adenosine Triphosphate
Uncoupling Protein 2

ASJC Scopus subject areas

  • Medicine(all)

Cite this

A radical explanation for glucose-induced β cell dysfunction. / Brownlee, Michael.

In: Journal of Clinical Investigation, Vol. 112, No. 12, 12.2003, p. 1788-1790.

Research output: Contribution to journalArticle

Brownlee, Michael. / A radical explanation for glucose-induced β cell dysfunction. In: Journal of Clinical Investigation. 2003 ; Vol. 112, No. 12. pp. 1788-1790.
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