scholarly journals β-Cell Uncoupling Protein 2 Regulates Reactive Oxygen Species Production, Which Influences Both Insulin and Glucagon Secretion

Diabetes ◽  
2011 ◽  
Vol 60 (11) ◽  
pp. 2710-2719 ◽  
Author(s):  
Christine A. Robson-Doucette ◽  
Sobia Sultan ◽  
Emma M. Allister ◽  
Jakob D. Wikstrom ◽  
Vasilij Koshkin ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Production ◽  
Uncoupling Protein ◽  
Reactive Oxygen ◽  
Glucagon Secretion ◽  
Uncoupling Protein 2 ◽  
Oxygen Species ◽  
Β Cell ◽  
Insulin And Glucagon Secretion ◽  
Species Production

Disruption of the uncoupling protein-2 gene in mice reveals a role in immunity and reactive oxygen species production

10.1038/82565 ◽  
2000 ◽  
Vol 26 (4) ◽  
pp. 435-439 ◽  
Author(s):  
Denis Arsenijevic ◽  
Hiroki Onuma ◽  
Claire Pecqueur ◽  
Serge Raimbault ◽  
Brian S. Manning ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Production ◽  
Uncoupling Protein ◽  
Reactive Oxygen ◽  
Uncoupling Protein 2 ◽  
Oxygen Species ◽  
Species Production

scholarly journals Uncoupling protein 2 regulates reactive oxygen species formation in islets and influences susceptibility to diabetogenic action of streptozotocin

2009 ◽  
Vol 203 (1) ◽  
pp. 33-43 ◽  
Author(s):  
Simon C Lee ◽  
Christine A Robson-Doucette ◽  
Michael B Wheeler
Keyword(s):  
Reactive Oxygen Species ◽  
Insulin Secretion ◽  
Cell Function ◽  
Uncoupling Protein ◽  
Plasma Concentrations ◽  
Reactive Oxygen ◽  
Glucagon Secretion ◽  
Uncoupling Protein 2 ◽  
Oxygen Species ◽  
The Impact

Currently, the physiological function of uncoupling protein-2 (UCP2) in pancreatic islets and its role in the development of diabetes is a matter of great debate. To further investigate the impact of UCP2 on diabetes development, we used streptozotocin (STZ) to experimentally generate diabetes in both wild-type (WT) and UCP2-knockout (UCP2KO) mice. While multiple low-dose STZ injections led to hyperglycemia development over a 14-day period in both WT and UCP2KO mice, we found the development of hyperglycemia to be significantly less severe in the UCP2KO mice. Measurement of insulin and glucagon secretion (in vitro), as well as their plasma concentrations (in vivo), indicated that UCP2-deficiency showed enhanced insulin secretion but impaired α-cell function. Glucagon secretion was attenuated, despite reduced insulin secretion after exposure to STZ, which together contributed to less severe hyperglycemia development in UCP2KO mice. Further experimentation revealed that UCP2-deficient α- and β-cells had chronically higher cellular reactive oxygen species (ROS) levels than the WT prior to STZ application, which correlated with increased basal β- and α-cell mass. Overall, we suggest that increased chronic ROS signaling as a result of UCP2-deficiency contributes to enhanced β-cell function and impairment of α-cell function, leading to an attenuation of STZ-induced hyperglycemia development.

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