[HTML][HTML] A radical explanation for glucose-induced β cell dysfunction

M Brownlee - The Journal of clinical investigation, 2003 - Am Soc Clin Investig
M Brownlee
The Journal of clinical investigation, 2003Am Soc Clin Investig
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 …
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
The Journal of Clinical Investigation