Key result
A high-fat diet did not worsen cardiac hypertrophy or left ventricular chamber enlargement in mice subjected to pressure overload, but preserved mitochondrial oxidative enzyme activities compared to a low-fat diet.
Why the study?
Does a high-fat diet affect the development of heart failure and mitochondrial oxidative enzyme activity in mice with pressure overload?
Does a high-fat diet affect the development of heart failure and mitochondrial oxidative enzyme activity in mice with pressure overload?
A high-fat diet preserves mitochondrial oxidative capacity without worsening cardiac hypertrophy in a mouse model of pressure overload-induced heart failure.
High-fat diet preserves mitochondrial enzymes without worsening hypertrophy in overloaded mice; leaves open translation to human HF models.
A high-fat diet can increase adiposity, leptin secretion, and plasma fatty acid concentration. In hypertension, this scenario may accelerate cardiac hypertrophy and development of heart failure but could be protective by activating peroxisome proliferator-activated receptors and expression of mitochondrial oxidative enzymes. We assessed the effects of a high-fat diet on the development of left ventricular hypertrophy, remodeling, contractile dysfunction, and the activity of mitochondrial oxidative enzymes. Mice (n = 10-12/group) underwent transverse aortic constriction (TAC) or sham surgery and were fed either a low-fat diet (10% of energy intake as fat) or a high-fat diet (45% fat) for 6 wk. The high-fat diet increased adipose tissue mass and plasma leptin and insulin. Left ventricular mass and chamber size were unaffected by diet in sham animals. TAC increased left ventricular mass (approximately 70%) and end-systolic and end-diastolic areas (approximately 100% and approximately 45%, respectively) to the same extent in both dietary groups. The high-fat diet increased plasma free fatty acid concentration and prevented the decline in the activity of the mitochondrial enzymes medium chain acyl-coenzyme A dehydrogenase (MCAD) and citrate synthase that was observed with TAC animals on a low-fat diet. In conclusion, a high-fat diet did not worsen cardiac hypertrophy or left ventricular chamber enlargement despite increases in fat mass and insulin and leptin concentrations. Furthermore, a high-fat diet preserved MCAD and citrate synthase activities during pressure overload, suggesting that it may help maintain mitochondrial oxidative capacity in failing myocardium.
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Chess et al. (2009) studied Heart failure with pressure overload (n=39). High-fat diet vs. Low-fat diet (10% of energy from fat) was evaluated on Left ventricular mass, chamber size, and mitochondrial oxidative enzyme activity. A high-fat diet did not worsen cardiac hypertrophy or left ventricular chamber enlargement in mice subjected to pressure overload, but preserved mitochondrial oxidative enzyme activities compared to a low-fat diet.
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