Abstract
Oxidative stress can impair mitochondrial function and fuel utilization and is closely linked with the development of insulin resistance in skeletal muscle in diabetes mellitus as well as fatty liver disease. In vitro data indicate that cellular levels of reactive oxygen species depend on the expression and activity of p53, which plays a key role in energy metabolism and as a crucial transcription factor for SCO cytochrome oxidase deficient homolog 2 (SCO2) and tumor p53-induced glycolysis and apoptosis regulator (TIGAR), which regulate mitochondrial respiration and glycolysis in cells. The aims of this study were: (1) to investigate whether exercise training could attenuate the development of oxidative stress in skeletal muscle in rats with diabetes mellitus (DM) and (2) to evaluate the potential role of p53 and its transcriptional targets in exercise-induced mitochondrial adaptation in skeletal muscle in rats with DM. Goto-Kakizaki (GK) rats, which develop type 2 DM (T2DM) early in life, were randomly divided into two groups: (1) subjected to regular exercise on a treadmill at 20m/min for 30–60min, 6days per week for 8weeks (GK exercising, n=7), and (2) rested controls (GK control, n=7). Exercise training increased serum adiponectin and decreased serum insulin and levels of glycosylated hemoglobin (P<0.05). Skeletal muscle GSH content and GSH:GSSG ratio increased in GK exercising rats vs GK controls (P<0.05). Skeletal muscle COX activity (P<0.05), mtDNA markers (P<0.01), and COXII protein levels (P<0.05) increased in response to exercise training. Exercise training decreased p53 protein levels and TIGAR expression in skeletal muscle (P<0.05), but SCO2 expression was unchanged. These data indicate that exercise training can attenuate oxidative stress and increase mitochondrial DNA content in skeletal muscle in rats with T2DM and that exercise-induced suppression of p53 and TIGAR expression may play a role in preventing oxidative stress in insulin resistance.
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