Cardiac remodeling (CR) occurs in response to certain types of aggression, such as pressure overload, and it can be clinically manifested by changes in size, shape and function of the heart. In the model of supravalvar aortic stenosis (SVAS) in rats, echocardiographic studies have shown that, after 2 and 6 weeks of SVAS induction, rats develop left ventricular hypertrophy, diastolic dysfunction and improvement of systolic function. After the 12th week the deterioration of systolic performance occurs and around the 20th week the signs of heart failure (HF) appear. Several factors, such as changes in energy metabolism, may contribute to cardiac dysfunction in the experimental model of SVAS. In the adult heart about 60-70% of the energy used in the contraction and relaxation process is obtained from the beta oxidation of fatty acids, and the contribution of the glycolytic pathway is around 30-40%. In pathological cardiac hypertrophy, with or without HF, change occurs in the use of myocardial energy substrate evidenced by increased glucose capture and utilization. In addition, there is downregulation of beta oxidation by reduction of proteins involved in the capture and oxidation of fatty acids and also an increase in metabolic stress sensors. The administration of a diet rich in unsaturated fatty acids could provide the ligand to stimulate an increase in the expression of proteins involved in fatty acid metabolism, allowing greater capture and utilization of lipids, reducing or delaying the metabolic dysfunction and the mechanical one that occur during the progression of pathological cardiac remodeling. There are few studies that evaluated the relationship among high-fat diet, energy metabolism and cardiac function in models of hypertrophy by pressure overload. There are no studies that evaluated the effect of hyperlipidic dietary treatment on energy metabolism and cardiac function after the establishment of ventricular hypertrophy accompanied by diastolic dysfunction. This study aims to test the hypothesis that the increase in the unsaturated fatty acid supply attenuates the metabolic alteration and the cardiac function impairment in rats with left ventricular hypertrophy and diastolic dysfunction by aortic stenosis. This attenuation is due to the increased expression of proteins involved in the lipid energy metabolism regulation.
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