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A radical explanation for glucose-induced β cell dysfunction

2003; American Society for Clinical Investigation; Volume: 112; Issue: 12 Linguagem: Inglês

10.1172/jci200320501

1558-8238

Michael Brownlee,

Adipose Tissue and Metabolism

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. 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 diabete