Exposure to cigarette smoke (ECS) not only increases the risk for cardiovascular disease, but also directly damages the myocardium. Experimental and clinical studies show that ECS is associated with myocardial dysfunction and hypertrophy, regardless of vascular factors. Little is known about the mechanisms involved in myocardial injury induced by ECS. Among these mechanisms are the changes in energy metabolism. In a normal heart, 60-90% of the ATP comes from the oxidation of fatty acids (FA). In pathological conditions, there are changes in the use of substrates, in mitochondrial biogenesis and finally the production of ATP, which may compromise cardiac morphology and function. Studies have shown that smoking can lead to insulin resistance, which in turn may compromise the cardiac bioenergetics. However, it is not known whether there is impairment of cardiac energy metabolism associated with insulin resistance induced by the ECS. Thus, the objectives of the study are to evaluate insulin resistance and pathways of glucose metabolism in the rat heart ECS and its association with cardiac morphofunctional variables. 60 animals allocated will be used in 2 groups: group of animals exposed to cigarette smoke (ECS), and group animals not exposed to cigarette smoke (C). After 2 months the animals will be subjected to: a) biochemical study to evaluate insulin resistance and cigarette exposure, b) echocardiographic study to assess morphological and functional; c) measurement of flow blood pressure; d) histological study using immunofluorescence to evaluate hypertrophy, angiogenesis and translocation of GLUT-4; e) Western blot to assess the expression of proteins involved in insulin resistance and glucose metabolism f) spectrophotometric evaluation to the activity of enzymes of energy metabolism and the amount of cardiac glycogen.
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