Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comparative Study
. 1992 Oct 21;116(1-2):39-45.
doi: 10.1007/BF01270567.

Carnitine palmitoyltransferase in the heart is controlled by a different mechanism than the hepatic enzyme

Affiliations
Comparative Study

Carnitine palmitoyltransferase in the heart is controlled by a different mechanism than the hepatic enzyme

G A Cook et al. Mol Cell Biochem. .

Abstract

Diminished sensitivity of hepatic carnitine palmitoyltransferase to inhibition by malonyl-CoA in the fasting and diabetic states is a well-recognized aspect of the regulatory mechanism for hepatic fatty acid oxidation. Inhibition of myocardial carnitine palmitoyltransferase by malonyl-CoA may play an important role in regulation of fatty acid oxidation in the heart, but there has been a discrepancy in data relating to changes in malonyl-CoA sensitivity of the myocardial carnitine palmitoyltransferase during fasting. Analysis of malonyl-CoA inhibition of myocardial carnitine palmitoyltransferase in fasting and fed states under a variety of conditions has indicated that under no condition could any difference be found in malonyl-CoA sensitivity that was attributable to fasting. Proteolysis of the outer carnitine palmitoyltransferase led to artifactual changes in sensitivity due to the appearance of partial inhibition. We have concluded that the sensitivity of myocardial carnitine palmitoyltransferase to malonyl-CoA does not change during fasting. Changes in fatty acid oxidation in the heart are probably due to changes in malonyl-CoA concentrations or to other inhibitors.

PubMed Disclaimer

Similar articles

Cited by

References

    1. FEBS Lett. 1984 Oct 29;176(2):381-4 - PubMed
    1. Biochim Biophys Acta. 1987 Dec 18;916(3):482-92 - PubMed
    1. Biochem J. 1980 Dec 15;192(3):955-8 - PubMed
    1. Annu Rev Biochem. 1980;49:395-420 - PubMed
    1. J Mol Cell Cardiol. 1985 Jun;17(6):619-25 - PubMed

Publication types