Reactive oxygen species are produced at low glucose and contribute to the activation of AMPK in insulin-secreting cells.

Details

Serval ID
serval:BIB_BB2BF65A0BBC
Type
Article: article from journal or magazin.
Collection
Publications
Title
Reactive oxygen species are produced at low glucose and contribute to the activation of AMPK in insulin-secreting cells.
Journal
Free Radical Biology and Medicine
Author(s)
Sarre A., Gabrielli J., Vial G., Leverve X.M., Assimacopoulos-Jeannet F.
ISSN
1873-4596 (Electronic)
ISSN-L
0891-5849
Publication state
Published
Issued date
2012
Volume
52
Number
1
Pages
142-150
Language
english
Abstract
Excess reactive oxygen species (ROS) production is thought to play a key role in the loss of pancreatic β-cell number and/or function, in response to high glucose and/or fatty acids. However, contradictory findings have been reported showing that in pancreatic β cells or insulin-secreting cell lines, ROS are produced under conditions of either high or low glucose. Superoxide production was measured in attached INS1E cells as a function of glucose concentration, by following in real time the oxidation of dihydroethidine. Minimal values of superoxide production were measured at glucose concentrations of 5-20 mM, whereas superoxide generation was maximal at 0-1 mM glucose. Superoxide generation started rapidly (15-30 min) after exposure to low glucose and was suppressed by its addition within minutes. Superoxide was totally suppressed by rotenone, but not myxothiazol, suggesting a role for complex I in this process. Indirect evidence for mitochondrial ROS generation was also provided by a decrease in aconitase activity. Activation of AMPK, a cellular metabolic sensor, and its downstream target ACC by low glucose concentration was largely inhibited by addition of MnTBAP, a MnSOD and catalase mimetic that also totally suppressed superoxide production. Taken together, the data show that low glucose activates AMPK in a superoxide-dependent, AMP-independent way.
Pubmed
Web of science
Open Access
Yes
Create date
17/02/2012 13:22
Last modification date
20/08/2019 15:29
Usage data