Obesity is a chronic metabolic disorder characterized by excessive adipose tissue accumulation in relation to lean tissue. Currently, it is known that the adipocyte receives influence of several substances and secrete numerous peptides, such as renin, angiotensinogen, angiotensin I (Ang-I) and II (Ang-II), angiotensin converting enzyme (ACE) and receptor type 1 angiotensin II (AT1), some of the renin-angiotensin system (RAS) components, which are regulated by the adiposity degree. Adipose tissue is considered an active endocrine, paracrine and autocrine organ with multiple functions, able to synthesize and release mediators that participate in many biological processes in different organs, including the heart. The heart is essentially composed of myocytes, nerves, vessels and interstitial matrix, the main component of matrix is collagen, predominantly type I and type III, being type I the most abundant. The components of RAS are also synthesized, in situ, in the heart and is not originally obtained from circulation. While circulating RAS exerts an acute and hemodynamic effect, myocardial tissue system is involved in long-lasting effects, such as cardiac remodeling, characterized, among others, by changes in interstitial collagen. Due to the deleterious association between saturated fatty acids and cardiovascular system, and due to the absence of studies that evaluated the relationship of obesity by saturated high-fat diet, collagen types I and III and myocardial RAS, the aim of this study is to test the hypothesis that obesity by high-fat diet, rich in saturated fatty acids, increases myocardial collagen I and III by activating AT1 receptor of RAS. To consolidate this precept, AT1 receptor will be blocked by losartan administration, which should, partially or fully, attenuate the changes in myocardial collagen I and III in obese rats.
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