This group also presented reduced levels of SCD, a key enzyme in the lipogenesis. In fact, in this set of animals the levels of triglycerides were increased. However, the high levels of triglycerides in this group do not represent a metabolic disorder – these animals do not present increased cholesterol and glucose values, for example. The result can be related to decreased lipogenesis and the time that blood was harvested for analysis. Although they were not analyzed in previous studies with AMPK/PPAR agonists, potential adverse effects related to exercise mimetics should be monitored carefully. Interestingly, the exercise mimetics group showed improved renal function by creatinine clearance test. Finally, we showed that all strategies reduced carcass fat, but with higher magnitude in the animals submitted to both exercise training and AMPK/PPAR agonists. This result suggests increased lipolysis and generation of energy by the oxidative metabolism, which is supported by the increased serum levels of triglycerides in this group. The significance of the reduction in the carcass fat is highlighted if we consider that there was no statistical difference among the groups in body weight. We also demonstrated that the ratio between protein expressions of phosphorylated and total acetyl-CoA carboxylase was increased in the three groups submitted to the treatments, which indicate inhibition of carboxylation of acetyl-CoA to malonyl-CoA in the biosynthesis of fatty acids. These results might explain the results from the carcass fat. In addition, these data reinforce the effectiveness of the exercise mimetics treatment because an AMPK downstream activity is the phosphorylation of acetyl-CoA carboxylase. In short, a beneficial effect of combination of exercise training and AMPK/PPAR agonists was observed in mdx mice. Although exercise training alone or alternatively its mimetics showed some improvement in skeletal muscle histology and aerobic capacity of mdx mice, the combination of both strategies seems more effective. In addition, our results suggest that a favorable protein turnover as well an improved efficiency of the oxidative metabolism might explain, at least in part, the observed functional improvements. It will be interesting to repeat these studies in other experimental models of muscular dystrophy. Although most dystrophic patients are not able to run, the animals in the present study are in the early stages of dystrophy, when many children would still be able to exercise. It would also be of interest to assess if the association of passive exercise and AMPK/ PPAR agonists have a comparable beneficial effect. Consequently, the incidence of ORG has increased over the last decade, and the epidemic of obesity has led to a progressive increase in number of cases of ORG in China. Thus, understanding the pathogenesis is crucial to develop new therapies for its prevention and treatment. Evidence shows that altered lipid metabolism, such as hyperlipidemia and increased free fatty acids, is an important characteristic of obesity and BAY-60-7550 contributes to renal lesions. Intracellular fatty acid-binding proteins are members of a multigene family encoding,15-kDa proteins, which allow the fatty acid to enter or exit the cellular cavity and thereby assist with the cell injury and death induced by the FAs. Interestingly, we previously demonstrated that lipid dysmetabolism in involved in the development of ORG, and heart-type fatty acid binding protein is especially up-regulated in the glomeruli.