BACKGROUND: Acylcarnitine (AC) transport dysfunction into the mitochondrial matrix is one of the pathophysiological mechanisms of type 2 diabetes mellitus (DM). The effect of an aerobic exercise (AE) program on this condition in obese subjects without DM is unclear. METHODS: A prospective, randomized, longitudinal, interventional study in a University Research Center involved a 10-week AE program in 32 women without DM and a body mass index (BMI) greater than 27 kg/m2. (cases n = 17; controls n = 15). The primary objective was to evaluate the influence of a controlled AE program on beta-oxidation according to modifications in short, medium, and long-chain ACs. Secondary objectives were to define the behavior of amino acids, and the correlation between these modifications with metabolic and anthropometric markers. RESULTS: The proportion of dropouts was 17% and 6% in controls and cases, respectively. In cases there was a significant reduction in total carnitine (30.40 (95% CI 28.2 to 35.6)) versus (29.4 (CI 95% 25.1 to 31.7), p = 0.0008) and long-chain AC C14 (0.06 (95% CI 0.05 to 0.08)) versus (0.05 (95% CI 0.05 to 0.09), p = 0.005) and in C18 (0.31 (95% CI 0.27 to 0.45)) versus (0.28 (95% CI 0.22 to 0.32), p = 0.03). Free fatty acid levels remained without change during the study in both groups. CONCLUSION: In conclusion, a controlled 10-week AE program improved beta-oxidation by reducing long-chain ACs. This finding highlights the importance that AE might have in avoiding or reverting lipotoxicity, and in consequence, improving insulin sensitivity and pancreatic beta cell functional reserve.

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