Submitted to: Circulation
Publication Type: Abstract only
Publication Acceptance Date: 7/20/2006
Publication Date: 10/31/2006
Citation: Okere, I.C., Young, M.E., Chess, D.J., McMahon, T.A., Ernsberger, P.R., Hoit, B.D., Chandler, M.P., Stanley, W.C. 2006. High fat/low carbohydrate diet attenuates left ventricular hypertrophy and prevents myosin heavy chain isoform switching induced by chronic hypertenstion [abstract]. Circulation. 114(18):667-668. Interpretive Summary:
Technical Abstract: A switch in the expression of myosin heavy chain isoform (MHC) alpha to beta is observed with left ventricular hypertrophy (LVH) and heart failure. This switch is associated with a defect in myocardial energy production and contractile dysfunction. Similar MHC isoform profile is observed in the fetal heart, which shares downregulation of fatty acid oxidation with LVH. We evaluated the hypothesis that preventing the downregulation of fatty acid oxidation with a high fat/low carbohydrate diet would prevent this switch. Method: 4 groups (n=10) of male Dahl salt-sensitive rats were fed diets composed of low fat/low salt (LF/LS, 10% of calories from fat), low fat/high salt (6% NaCI, (LF+HS)), high fat/low salt (HF/LS, 60% of calories from fat), and high fat/high salt (HF+HS). Tail cuff blood pressures and cardiac function (by echocardiography) were evaluated before initiation of feeding and after 12 weeks on the diet. Gene expressions for MHC alpha and beta, and atrial natriuretic peptide were measured by rtPCR. Histological assessment of myocyte cross-sectional area was also performed. Results: High salt induced similar elevation in blood pressures among groups. Hypertension caused significant increases in LV mass, myocyte cross sectional area, an 11-fold induction of ANF, a decline in ejection fraction, and switching of MHC alpha to MHC beta in the LF/HS fed groups. High fat prevented hypertension-induced decline in contractile function and prevented gene induction of ANF and MHC isoform switching. Conclusion: High fat feeding prevented hypertension induced cardiac contractile dysfunction, LVH, and prevented myosin heavy chain isoform switching, implying an important role for fatty acids in determining cardiac contractile and hypertrophic phenotypes in hypertensive heart disease.