Estresse oxidativo cardíaco na condição de resistência à obesidade

Abstract

Resistance to Obesity is associated with the complex interaction of stringent and environmental factors, conferring the ability to gain mass gain and body fat deposition, even when eating high-calorie diets. Considering that there are numerous gaps in the literature on the metabolic processes that explain Resistance to Obesity, specifically in relation to oxidative stress, the purpose of the study was to investigate whether obesity- resistant rats develop elevated reactive oxygen species in cardiac tissue. Methods: Wistar rats were initially randomized into two groups: Control (C) and High-fat diet (HFD). The HFD group was further divided into the Obese (Ob) and Obesity-Resistant (OR) groups based on body weight gain (upper 1/3 for Ob; lower 1/3 for OR) after 4 weeks on HFD. Rats were sacrificed at the 14th week, and serum and organs were collected. Nutritional assessment, food profiles, histological analysis, comorbidities, and cardiovascular characteristics were determined. Results: Body mass showed a significant difference between the standard diet and high-fat diet groups in the 4th week of the experimental protocol, characterizing obesity. In the 4th week, after the characterization of Resistance to Obesity, there was a significant difference in body mass between groups C, Ob and ROb. Ob and ROb groups showed a significant increase in caloric intake in relation to the C. Ob group showed a significant increase in final body mass, retroperitoneal fat pad, sum of corporal fat deposits and in reactive oxygen species, in relation to groups C and Rob. The area under the glycemic curve (AUC), the insulin resistance index and the baseline blood glucose were increased in the Ob group compared to the C group. Total cardiac mass, cross-sectional area (LV), collagen fraction (LV), cholesterol and leptin levels were significantly higher in the Ob and Rob groups compared to the C group. The high-fat diet, in obesity-resistant rats, promoted cardiac hypertrophy without reactive oxygen species alterations.