Brownlee 2003 J Clin Invest
Has title::Brownlee M (2003) A radical explanation for glucose-induced beta cell dysfunction. J Clin Invest 112:1788-90. https://doi.org/10.1172/JCI20501 |
Β» [[Has info::PMID: 14679173 Open Access]]
Was written by::Brownlee M (Was published in year::2003) Was published in journal::J Clin Invest
Abstract: [[has 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.]]
β’ Bioblast editor: has 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 (2024).
- Gnaiger E (2024) Complex II ambiguities β FADH2 in the electron transfer system. J Biol Chem 300:105470. https://doi.org/10.1016/j.jbc.2023.105470 - Β»Bioblast linkΒ«
Labels:
Enzyme: Enzyme::Complex II;succinate dehydrogenase