Obesity involves co-morbidities as dyslipidemia, cardiovascular disease, insulin resistance and type 2 diabetes. One characteristic of obesity is the propensity for increased circulating fatty acids. However, a loss of synchronization between fatty acid availability and oxidation would result in accumulation of fatty acid derivatives in non specific tissue such the cardiomyocyte, inducing lipotoxicity that is associated with contractile dysfunction and heart failure. It is also observed mitochondrial dysfunction playing key role in cardiac hypertrophy and failure, that can indicate defects at specific sites in electron transport chain (1, 2, 3, 4). The aim of the study was to investigate how lipid and glucose metabolic alterations affect the ventricular contractile function in mice fed high fat diet, through mitochondrial bioenergetics. After weaning, mouse C57Bl/6 received diet containing 7% (C) or 19% (HF) of soybean oil, until 135 days old. Food intake and body mass were monitored, and glucose tolerance test was realized. At 135 days, body composition was evaluated by Dual-energy X-ray Absorptiometry (DEXA) and after, animals were sacrificed by exsanguination. Lipid profile, leptin, insulin, HOMA-IR and the adiposity index were evaluated. The heart, the pancreas and intraabdominal adipose tissue were collected, weighted and processed to morphological analysis. Left ventricular myocardial fibers were used to analyze mitochondrial respiration by technique of high resolution respirometry. Cardiac hemodynamic was evaluated by Langendorff technique of isolated heart perfusion and proteins related to cardiomyocytes bioenergetics (CPT1, UCP2, GLUT1, GLUT4, AMPK and pAMPK) were analyzed by Western blotting. The group HF presented differences in adiposity (130%) with adipocyte hypertrophy (200%), , glucose intolerance, hyperinsulinemia (80%), insulin resistance and pancreatic islet hypertrophy (200%); hyperleptinemia (22%), increase of triglycerides (49%), LDL (29%) and VLDL (51%), without difference in food intake. The hypertrophic cardiomyopathy observed reflected in hemodinamic alterations as increased contractility (78%), higher ventricular pressure (63%) and impaired diastolic function (-36%). Oxidation of carbohydrates (-47%) and fatty acids (-60%) was decreased in cardiomyocytes, however, the expression of proteins co-related to cardiomyocytes bioenergetics did not differ between the groups. Obesity induced metabolic disorders in series, leading to dyslipidemia, type 2 diabetes mellitus, besides impairment of mitochondrial oxidative capacity and cardiac hypertrophy, causing hemodynamic dysfunction. However, these alterations are dissociated of energetic cardiac sensor.