Consistent with this, Selleck 17DMAG in our study, only the case group had a decrease in long-chain AC as a result of improved beta-oxidation. A critical factor that

strengths the AE program in the case group, was that all the anthropometric and metabolic variables where modified according to what is already well known [37–39]. As well, amino acids, ornithine and tyrosine decreased as previously described by AE [40]. Another important finding in our study was that in the case group medium-chain AC C8 and C5 increased at the end of the exercise program. Unlike long-chain AC, medium chain AC did not depend on CPT1 for transfer to the mitochondrial matrix. This would reinforce the theory that improvement in beta-oxidation occurs mainly as a result of an increase Pitavastatin in CPT1 activity. Recent studies agree with this finding, suggesting that intermediate products such as beta-oxidation

of medium-chain AC accumulate in patients with type 2 DM, reflecting that a more complex beta-oxidation defect may be present; this abnormality was not reversed by the AE program our participants underwent [31, 35, 41]. It could be that a more intense AE program, with a greater length of time, in an older population and with insulin resistance could improve this defect in beta-oxidation in subjects who are obese or have diabetes. If the mitochondrial capacity of beta-oxidation is a permanent or reversible defect is a matter of controversy. NADPH-cytochrome-c2 reductase Recent studies have found that mitochondrial beta-oxidation is reduced in patients with type 2 DM and that this abnormality is reversible [42, 43]. In a group of 10 patients with obesity and type 2 DM, Toledo et al.

(2007), in skeletal muscle biopsies, showed an improvement in beta-oxidation after a moderate 16-week AE program. In another study in 21 obese subjects undergoing a 16-week AE program, muscle biopsies at the end of the study identified an increased number of mitochondria and an increased amount of lipid droplets consistent with the beneficial metabolic effects. Our results show that a controlled 10-week AE program was able to improve, in the case group, beta-oxidation. Conclusions A 10-week AE program led to well known anthropometric and biochemical modifications in a young group of obese women without DM, improved beta-oxidation by decreasing long-chain ACs probably due to an increase in CPT1 function, being this a consequence of the physical activity and the weight loss that occurred as a direct result of the AE program. These findings warrant longer-term studies to analyze their effects on long and medium-chain AC and the permanence of these modifications after stopping exercise. So far our results suggest that a long term AE program might likely improve lipotoxicity and, consequently, insulin action and pancreatic beta cell functional reserve. Acknowledgements We wish to thank Selleck MRT67307 Sergio Lozano-Rodríguez, for his critical reading of the manuscript.