Defective lipid metabolism in the failing heart

Benjamin Wittel; James F. Spann

doi:10.1172/JCI105868

^{Department of Pathology, Duke University Medical Center, Durham, North Carolina 27706}

^{Cardiology Branch, National Heart Institute, Bethesda, Maryland 20014}

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^{Department of Pathology, Duke University Medical Center, Durham, North Carolina 27706}

^{Cardiology Branch, National Heart Institute, Bethesda, Maryland 20014}

Find articles by Spann, J. in: PubMed | Google Scholar

Published in Volume 47, Issue 8 on August 1, 1968
J Clin Invest. 1968;47(8):1787–1794. https://doi.org/10.1172/JCI105868.
© 1968 The American Society for Clinical Investigation

Published August 1, 1968 - Version history

The metabolism of long chain fatty acids was investigated in the failing heart of guinea pigs with chronic constriction of the ascending aorta. Homogenates prepared form failing hearts exhibited (a) a decreased capacity to oxidize palmitic acid (failure = 0.50 ± 0.06 μmole/g of protein per 20 min; control = 1.09 ± 0.10); (b) a reduced level of carnitine, a myocardial constituent which serves to control the oxidation rate of long chain fatty acids in the heart (failure = 0.91 ± 0.10 μmole/g wet weight; control = 1.69 ± 0.10); and (c) an increased rate of palmitate incorporation into triglycerides and lecithin. Exogenous carnitine effected a restoration of the defective palmitate metabolism of the homogenates towards normal. In contrast to long chain fatty acid oxidation, glucose oxidation by the failing heart was not impaired. As a consequence of this selective lesion in energy substrate utilization, the failing heart might be forced to rely on substrates other than long chain fatty acids for its major energy supply.