A high-fat diet increases adiposity but maintains mitochondrial oxidative enzymes without affecting development of heart failure with pressure overload
DJ Chess, RJ Khairallah, KM O'Shea… - American Journal …, 2009 - journals.physiology.org
DJ Chess, RJ Khairallah, KM O'Shea, W Xu, WC Stanley
American Journal of Physiology-Heart and Circulatory Physiology, 2009•journals.physiology.orgA 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 …
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 …
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 (∼70%) and end-systolic and end-diastolic areas (∼100% and ∼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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