Efeitos da dieta hiperproteica sobre a disfunção mitocondrial na Insuficiência Cardíaca induzida pela sobrecarga de pressão em ratos

Abstract

Despite aggressive diagnosis and treatment, HF remains a major clinical problem and a huge burden on the health care system. Among all cardiovascular diseases, heart failure is responsible for the high morbidity and mortality rates. At present there is limited information regarding the effects of dietary macronutrient composition and heart failure. There is a clear need to develop recommendations for dietary macronutrients for people who are “at risk” for the development of heart failure (eg, patients with coronary heart disease, hypertension, left ventricular hypertrophy, diabetes), and for patients with established heart failure. We assessed the effects of a high protein diet on the development of heart failure characterized by cardiac hypertrophy, impaired mitochondrial oxidative metabolism and contractile dysfunction induced by transverse aortic constriction (TAC) in rats. In this study, for the first time, we demonstrated the effects of high protein diet for 14 and 22 weeks on mortality, cardiac function and mitochondrial function from both subpopulations (interfibrillar and Subsarcolemal) of rats with or without heart failure. We showed that high protein diet increased mortality in heart failure animal whereas it did not increase mortality in SHAM animals. Mitochondrial analyses showed that high protein diet decreased bioenergetics (i.e. β-oxidation), increased calcium uptake and permeability transition pore after 14 weeks. Despite mitochondrial function impairment at 14 weeks, high protein diet did not affect cardiac function analyzed by echocardiography, in both Sham protein and TAC protein groups when compared to control. Besides, we showed that high protein diet induced weight loss in TAC animals at 14 weeks without changing any other parameter evaluated. The animals at 22 weeks did not show weight loss. It seems that high protein diet affects mitochondrial function in heart failure animals, decreasing .β-oxidation and increasing mortality.