Submitted to: Hypertension
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/25/2006
Publication Date: 10/23/2006
Citation: Okere, I.C., Young, M.E., McElfresh, T.A., Chess, D.J., Sharov, V.G., Sabbah, H.N., Hoit, B.D., Ernsberger, P., Chandler, M.P., Stanley, W.C. 2006. Low carbohydrate/high-fat diet attenuates cardiac hypertrophy, remodeling, and altered gene expression in hypertension. Hypertension. 48:1116-1123. Interpretive Summary: Factors that increase risk for heart disease often go hand-in-hand. These include increased blood pressure (hypertension) and high lipid (fat) levels in the blood (known as dyslipidemia). This study investigated whether a high-fat diet (similar to the Atkins diet) influenced the heart disease associated with hypertension. Somewhat surprisingly, we found that a high-fat diet appeared to improve heart function in an animal model of hypertension. The results suggest that the Atkins diet may not accelerate heart disease progression, at least in the short term.
Technical Abstract: The effects of dietary fat intake on the development of left ventricular hypertrophy and accompanying structural and molecular remodeling in response to hypertension are not understood. The present study compared the effects of a high-fat versus a low-fat diet on development of left ventricular hypertrophy, remodeling, contractile dysfunction, and induction of molecular markers of hypertrophy (ie, expression of mRNA for atrial natriuretic factor and myosin heavy chain beta). Dahl salt-sensitive rats were fed either a low-fat (10% of total energy from fat) or a high-fat (60% of total energy from fat) diet on either low-salt or high-salt (6% NaCl) chow for 12 weeks. Hearts were analyzed for mRNA markers of ventricular remodeling and activities of the mitochondrial enzymes citrate synthase and medium chain acyl-coenzyme A dehydrogenase. Similar levels of hypertension were achieved with high-salt feeding in both diet groups (systolic pressure of approximately 190 mm Hg). In hypertensive rats fed low-fat chow, left ventricular mass, myocyte cross-sectional area, and end-diastolic volume were increased, and ejection fraction was decreased; however, these effects were not observed with the high-fat diet. Hypertensive animals on low-fat chow had increased atrial natriuretic factor mRNA, myosin heavy chain isoform switching (alpha to beta), and decreased activity of citrate synthase and medium chain acyl-coenzyme A dehydrogenase, which were all attenuated by high-fat feeding. In conclusion, increased dietary lipid intake can reduce cardiac growth, left ventricular remodeling, contractile dysfunction, and alterations in gene expression in response to hypertension.