학술논문

MITOCHODRIAL FUNCTION AND OXIDATIVE STRESS IN KIDNEY FROM RATS WITH METABOLIC SYNDROME.
Document Type
Article
Source
FASEB Journal. Apr2008 Supplement S2, Vol. 22, p710-710. 1p.
Subject
Language
ISSN
0892-6638
Abstract
Free fatty acids (FFA) release from adipose tissue where the lipolytic activity is higher due to insulin resistance, could be a link between obesity and renal disease in a model of metabolic syndrome (MS). Objetive: To elucidate the mechanism by which FFA affects the transmembranal potential and reactive oxygen species (ROS) generation in isolated mitochondria from kidney of rats with MS. Methods: MS was induced in Wistar rats by high sucrose intake during 24 weeks. Results: Mitochondria from kidney of MS animals have a reduced transmembrane potential oxidizing succinate (5mM) as compared with mitochondria from control animals. The addition of 30 μM oleic acid (OA) as a FFA, induced a proton leak and reduced the potential by 50% in both mitochondria. This proton leak can be mediated by UCP2, an uncoupler protein which it was overexpressed in mitochondria from MS. Although the pre-incubation of mitochondria with GDP (50 μM), an inhibitor of UCP1 (isoform of UCP2), did not affect the proton leak induced by OA. The addition of carboxyatractyloside (1 μM), an inhibitor of adenine nucleotide translocase, increase the transmemranal potencial of both mitochondria but with a great magnitude in mitochondria from MS. The rate of mitochondria ROS generation oxidizing succinate was increased in MS. This rate was increased more, when OA was added, in mitochondria from MS animals. [ABSTRACT FROM AUTHOR]