Brownlee 2003 J Clin Invest
|Brownlee M (2003) A radical explanation for glucose-induced beta cell dysfunction. J Clin Invest 112:1788-90. https://doi.org/10.1172/JCI20501|
Abstract: The development of type 2 diabetes requires impaired beta 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 beta cells exposed to hyperglycemia could prevent a positive feed-forward loop of glucotoxicity that drives impaired glucose tolerance toward frank type 2 diabetes.
• Bioblast editor: Gnaiger E
Correction: FADH2 and Complex II
- FADH2 is shown as the substrate feeding electrons into Complex II (CII). This is wrong and requires correction - for details see Gnaiger (2023).
Enzyme: Complex II;succinate dehydrogenase