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Papers In Press, published online ahead of print October 16, 2003
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Pharmacology and Therapeutical Chemistry, University of Barcelona, Barcelona E-08028
Corresponding Author: mvazquezcarrera{at}ub.edu
A decrease of mitochondrial DNA (mtDNA) content has been related to the pathogenesis of type 2 diabetes mellitus. In this study we show increased expression of the peroxisome proliferator-activated receptor-a (PPARa) and its target genes involved in fatty acid metabolism in skeletal muscle of Zucker Diabetic Fatty (ZDF) (fa/fa) rats. In contrast, the mRNA levels of genes involved in glucose transport and utilization (GLUT4 and phosphofructokinase) were decreased, whereas the expression of pyruvatedehydrogenase kinase 4 (PDK-4), which suppresses glucose oxidation, was increased. The shift from glucose to fatty acids as the source of energy in skeletal muscle of ZDF rats was accompanied by a reduction in the expression of two genes of the ETC encoded by mtDNA. Subunit 1 of complex I (NADH dehydrogenase subunit 1, ND1) showed a reduction in mRNA (68%, P<0.05) and protein levels, whereas a 41% reduction (P<0.02) was observed in the mRNA levels of the subunit II of complex IV (cytochrome c oxidase II, COII). The transcript levels of PPARg Coactivator 1 (PGC-1), which is involved in mitochondrial biogenesis and respiration, showed a 41% reduction (P<0.05). Treatment with the thiazolidinedione troglitazone (30 mg/kg/day) for 15 days reduced insulin values and reversed the increase in PDK-4 mRNA levels, suggesting improved insulin sensitivity. In addition, troglitazone treatment restored ND1 and PGC-1 expression in skeletal muscle. These results suggest that the thiazolidinedione troglitazone, by restoring the expression of these genes may avoid mitochondrial metabolic derangement resulting from inhibition of the ETC that occur during the development of diabetes mellitus 2 in skeletal muscle
Revised on August 1, 2003
Accepted on October 2, 2003
Impaired expression of the mitochondrial DNA-encoded gene NADH dehydrogenase subunit 1 and PPAR
coactivator-1 in skeletal muscle of ZDF rats: restoration by troglitazone treatment
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