Background: Obesity is a risk factor for medical complications, including the cardiovascular system. There is limited information on collagen in the heart in obesity. Our previous study showed decreased protein levels of myocardial collagen type I in obese rats fed a high-fat diet for 34 weeks. However, the mechanisms responsible for low levels are not fully elucidated. Objective: The purpose of this study was to test the hypothesis that the reduction in collagen type I is associated with increased metalloproteinase-2 (MMP-2) activity, which is linked to elevated leptin in the myocardium of obese rats. Methods: Thirty-day-old male Wistar rats were randomized into two groups, control (standard diet) and obese (high-fat diet), and fed for 34 weeks. The general animal characteristics and metabolic and endocrine profiles were evaluated. Myocardial protein expressions of collagen I, leptin, tissue inhibitors of metalloproteinases (TIMP), and MMP-2 activity were assessed. Pearson correlation was employed to determine the associations between variables. The level of significance was 5%. Results: The obese animals had increased adiposity index compared to control. Comorbidities such as glucose intolerance, hyperinsulinemia, insulin resistance, hyperleptinemia, and hypertension were observed in obese rats. Obesity reduced collagen I, TIMP-1, and TIMP-2, and it increased leptin and MMP-2 in the myocardium. There was a negative correlation between collagen I and MMP-2 and a positive correlation between leptin and MMP-2. Conclusion: The hypothesis was confirmed; the reduction in collagen type I is associated with increased MMP-2 activity and leptin expression in the myocardium of obese rats.
Obesity is a chronic metabolic disease characterized by an excessive adipose tissue accumulation. 1 It is considered a global epidemic and a major public health problem, 2 since this disease can lead to nutritional, metabolic, hormonal, and cardiovascular changes, increasing the population's morbidity and mortality, and reducing life expectancy. [3][4][5] The literature reports that the cause of main obesity, currently, is the inadequate dietary habits, with increased carbohydrate and/or fat consumption. 6,7 However, some individuals seem to present resistance to the development of obesity. Within this context, experiments using animals fed with a high-fat diet try to understand the pathophysiological susceptibility of obesity-resistant individuals to cardiometabolic diseases. [8][9][10]
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