BackgroundThe aim of the present study was to evaluate the protective effect of concurrent exercise in the degree of the insulin resistance in mice fed with a high-fat diet, and assess adiponectin receptors (ADIPOR1 and ADIPOR2) and endosomal adaptor protein APPL1 in different tissues.MethodsTwenty-four mice were randomized into four groups (n = 6): chow standard diet and sedentary (C); chow standard diet and simultaneous exercise training (C-T); fed on a high-fat diet and sedentary (DIO); and fed on a high-fat diet and simultaneous exercise training (DIO-T). Simultaneously to starting high-fat diet feeding, the mice were submitted to a swimming exercise training protocol (2 x 30 minutes, with 5 minutes of interval/day), five days per week, for twelve weeks (90 days). Animals were then euthanized 48 hours after the last exercise training session, and adipose, liver, and skeletal muscle tissue were extracted for an immunoblotting analysis.ResultsIR, IRs, and Akt phosphorylation decreased in the DIO group in the three analyzed tissues. In addition, the DIO group exhibited ADIPOR1 (skeletal muscle and adipose tissue), ADIPOR2 (liver), and APPL1 reduced when compared with the C group. However, it was reverted when exercise training was simultaneously performed. In parallel, ADIPOR1 and 2 and APPL1 protein levels significantly increase in exercised mice.ConclusionsOur findings demonstrate that exercise training performed concomitantly to a high-fat diet reduces the degree of insulin resistance and improves adipoR1-2/APPL1 protein levels in the hepatic, adipose, and skeletal muscle tissue.

mone-sensitive lipase (HSL) have the capacity for TG degradation by cleaving the ester bond, governing the lipolysis pathway in adipose tissue [ 6 ]. Adipose tissue lipolysis has received much attention over the past 10 years because of its altered regulation in obesity. Studies have suggested that obesity is associated with changes in gene expression in adipocytes with diff erent metabolic pathways and in diff erent organs and tissues, resulting in various metabolic actions and molecular signals [ 7 ] , and is closely associated with the low-grade chronic infl ammatory response [ 2 ]. These biochemical and molecular changes involve the participation of a number of molecules as transcription factors, infl ammatory mediators, and the formation of reactive oxygen species (ROS). ROS are chemically reactive molecules that are produced during normal metabolism of oxygen and play important roles in cell signaling and Authors J. M.