Loss of UCP2 attenuates mitochondrial dysfunction without altering ROS production and uncoupling activity.

ABSTRACT: Although mitochondrial dysfunction is often accompanied by excessive reactive oxygen species (ROS) production, we previously showed that an increase in random somatic mtDNA mutations does not result in increased oxidative stress. Normal levels of ROS and oxidative stress could also be a result of an active compensatory mechanism such as a mild increase in proton leak. Uncoupling protein 2 (UCP2) was proposed to play such a role in many physiological situations. However, we show that upregulation of UCP2 in mtDNA mutator mice is not associated with altered proton leak kinetics or ROS production, challenging the current view on the role of UCP2 in energy metabolism. Instead, our results argue that high UCP2 levels allow better utilization of fatty acid oxidation resulting in a beneficial eff

SUBMITTER: Kukat A 

PROVIDER: S-EPMC4063685 | biostudies-literature | 2014 Jun

REPOSITORIES: biostudies-literature