Abstract

This editorial refers to ‘High intake of saturated fat, but not polyunsaturated fat, improves survival in heart failure despite persistent mitochondrial defects’ by T.F. Galvao et al. , doi:10.1093/cvr/cvr258. Galvao et al. 1 compare the effects of two high-fat diets, both 45% kcal but sourced from either polyunsaturated fatty acids (PUFA; linoleic and α-linolenic acids) or saturated fat (palmitate and stearate) in a male δ-sarcoglycan null Bio TO2 hamster model of heart failure. Surprisingly, the heart failure hamsters fed the diet high in saturated fat showed increased survival compared with hamsters fed a diet high in PUFA or the control standard diet (12% kcal from fat). Importantly, in all three diet groups, the hamsters developed dysfunction at both the left ventricle and cardiac mitochondria levels. Despite the lack of a cardiac function phenotype, the PUFA-fed hamsters showed elevated Ca2+-induced mitochondrial permeability transition pore opening rates compared with both the saturated fat and standard fed hamsters. The clear distinction in obesity effects differentially driven by high-fat diets from different lipid sources, in the context of heart failure, has not been previously studied. The present study is important because it reveals the strong impact of fat source on cardiovascular events and survival rates in the setting of existing heart failure. A diet high in saturated fat promotes obesity by stimulating an inflammatory response that can induce cardiac concentric hypertrophy and alter the stress response.2 Obesity resulting either from saturated or PUFA …

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call