Efeitos do treinamento físico na adiposidade visceral, tecido adiposo marrom e parâmetros metabólicos de ratos Wistar alimentados com dieta hiperlipídica

Abstract

Obesity is a multifactorial disease that produces various metabolic disorders through the local and systemic inflammatory response occasioned by the pathological remodeling of visceral white adipose tissue (WAT). Furthermore, the activation of inflammatory pathways and the constant obesogenic state caused by the consumption of high-fat diet changes the morphology and function of the brown adipose tissue (BAT), a notable metabolic sink that oxidizes different energetic substrates in the form of heat and contributes to the regulation of the body mass and energy homeostasis. Notwithstanding, physical training is a non-pharmacological tool capable of decreasing the negative consequences of obesity and maintaining the metabolic flexibility of different peripheral tissues through decreasing visceral adiposity. Therefore, the purpose of this study was to investigate the effects of physical training on BAT mass, visceral adiposity and on metabolic parameters of Wistar rats fed a high-fat diet. First, male adult Wistar rats were separated within a control group fed a standard diet (CTR) and obese fed a high-fat diet (OB). After 12 weeks of obesity induction, the animals were subdivided into four groups: sedentary control group (CTR-SED), trained control group (CTR-TR), sedentary obese (OB-SED) and trained obese (OB-TR). The animals of the trained groups (CTR-TR and OB-TR) were submitted to physical training by swimming modality for eight weeks, in which each session of physical exercise was composed of 60 minutes of duration, frequency of 3 times a week, and intensity equivalent between 3 to 5% of the animal's body mass. The morphology of the epididymal fat (visceral WAT) was verified through histological analysis; visceral adiposity by weighing the deposits of epididymal, retroperitoneal and mesenteric WAT; the mass of the interscapular BAT was measured by weighing on an analytical balance and the glycogen and lipid content in the liver and soleus muscle were obtained using previously established methods in the literature. In the results, we observed that obesity (OB-SED) increased body mass, visceral adiposity, promoted adipocyte hypertrophy, deposition of ectopic lipids in the liver, reduced hepatic glycogen content and increased BAT relative mass. Physical training attenuated body mass increase, intraperitoneal adiposity, and adipocyte hypertrophy; however, was not efficient in reducing liver lipid content and increasing glycogen stores. Besides, physical training independent of the energy diet increased the relative mass of BAT, reduced the overlap of visceral fat on brown fat, and showed a negative correlation with the content of liver lipids. In summary, we conclude that physical training reduces weight gain and intraperitoneal adiposity in obese animals; however, these effects are not accompanied by changes in the metabolic flexibility of peripheral tissues in using fatty acids and glucose during cell activity. Furthermore, physical training and a high-fat diet are effective in increasing the mass of BAT, however, we do not know if this morphometric modification caused a thermogenic signature (expression of uncoupling protein 1 - UCP1) or whitening of brown adipocytes. Thus, further studies are needed to verify the biochemical and morphological adaptations of WAT and BAT in obese animals submitted to physical training.