High intake of saturated fat, but not polyunsaturated fat, improves survival in heart failure despite persistent mitochondrial defects

Abstract

These results show that a high intake of saturated fat improves survival in heart failure compared with a high PUFA diet or low-fat diet, despite persistent mitochondrial defects.

Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies

“…␦-Sarcoglycan null hamsters, a rodent model of dilated cardiomyopathy that exhibits decreased mitochondrial oxidative capacity and is responsive to nutritional and metabolic therapies, displayed distinct effects to the IFM subpopulation. These effects included a decrease in mitochondrial yield and direct impact on Ca 2ϩ -induced mPTP (37,38). These data are in agreement with others using cardiomyopathic hamsters in a time course analyses in which defective oxidative phosphorylation was confined to the IFM subpopulation.…”

“…Among these insights has been the recognition that in cardiac muscle, mitochondria exist in a number of different subcellular locales. This phenomenon has been corroborated in numerous mammalian species including mouse, rat, muskrat, guinea pig, hamster, rabbit, dog, pig, monkey, cow, and human (22,37,46,77,84,87,118,119,124,134). This phenomenon is consistent with the evaluation of other noncardiac cells such as neurons where functional heterogeneity between dendritic, somatic, axonal, and presynaptic segments due to variations in energy demands and calcium (Ca 2ϩ ) signaling dynamics are associated with structural and biochemical differences in mitochondria situated in a particular neuronal region.…”

Differential effects of high-fat diet on myocardial lipid metabolism in failing and nonfailing hearts with angiotensin II-mediated cardiac remodeling in mice

“…Finally, the results of the present study do not provide information on the effect of high-fat diet on global mitochondrial function. Fatty acid and glucose oxidation are an integral part of energy metabolism in mitochondria, which undergo a number of functional and structural alterations during the development of heart failure (15).…”

Marine n3 polyunsaturated fatty acids enhance resistance to mitochondrial permeability transition in heart failure but do not improve survival

“…There is growing evidence to support a causal role for mitochondrial dysfunction in the progression of heart failure. Heart failure induced by infarction, chronic hypertension, or genetic ␦-sarcoglycan deficiency results in mitochondrial pathology as evidenced by impaired oxidative phosphorylation and ATP production and enhanced susceptibility to stress-induced mitochondrial permeability transition (MPT) (1,11,21,23). MPT occurs with the formation and opening of the MPT pore and is generally considered to be a catastrophic event that collapses the proton motive force and causes mitochondrial swelling, cessation of ATP production, and efflux of matrix proteins that can trigger apoptotic pathways (16,40,41).…”