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(2008)
Reduced antioxidant capacity and diet-induced atherosclerosis in uncoupling protein-2-deficient mice
- Publisher
- Wiley Subscription Services, Inc., A Wiley Company
- Copyright
- Copyright © 2009 International Union of Biochemistry and Molecular Biology, Inc.
- ISSN
- 1521-6543
- eISSN
- 1521-6551
- DOI
- 10.1002/iub.188
- pmid
- 19514063
- Publisher site
- See Article on Publisher Site
Abstract
Mitochondrial uncoupling of oxidative phosphorylation may serve a variety of purposes such as the regulation of substrate oxidation, free radical production (a major by‐product of mitochondrial respiration) and ATP production and turnover. As regulators of energy expenditure and antioxidant defenses, uncoupling proteins would seem to offer an attractive mechanism by which to explain the control of body weight, resting metabolic rate and aging. As a result, the discovery of UCP1 homologues has led to an impressive number of publications. However, 10 years after their identification, no consensus has been found concerning the function of UCP homologues, and there are controversies as to whether or not they even have physiologically significant uncoupling activity. Here, we discuss a potential new function for UCP2, as a carrier involved in the coupling between glucose oxidation and mitochondrial metabolism. © 2009 IUBMB IUBMB Life 61(7): 762–767, 2009
Journal
IUBMB Life – Wiley
Published: Jul 1, 2009
Keywords: uncoupling protein; mitochondria; carrier; glucose and fatty acid oxidation; metabolism