J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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A more recent version of this article appeared on November 1, 2004

Papers In Press, published online ahead of print September 1, 2004
J. Lipid Res., doi:10.1194/jlr.M400237-JLR200
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Submitted on June 18, 2004
Revised on August 18, 2004
Accepted on August 20, 2004

Demonstration of reverse fatty acid transport from rat cardiomyocytes

Byung-Hyun Park, Young Lee, Marlei Walton, Laurence Duplomb, and Roger H. Unger

Internal Medicine, UT Southwestern Medical Center at Dallas, Dallas, TX 75390-8854

Corresponding Author: roger.unger{at}utsouthwestern.edu

Abstract Fatty acids (FA) flow from adipocytes to nonadipose tissues during fasting and exercise and normally are fully oxidized. To determine if nonadipose tissues can export unoxidized FA when FA influx exceeds oxidation, neonatal cardiomyocytes were cultured in 1 mCi 14C-palmitate in the presence of etomoxir to block oxidation. The cells took up and stored 25% of the radioactivity as 14C-TG in 12 hours, but 4.5% of the label was released in 3 hours and co-migrated with 14C-palmitate. Both uptake and release of radioactivity were increased by insulin and reduced by the nonspecific inhibitors of FA transporters, phloretin and DIDS. Perfused hearts from etomoxir-treated lean rats released 221 ± 59 nmoles/10 min of FA. Hearts from high fat-fed lean rats released 366 ± 172 nmoles/10 min (p<0.05). Hearts from obese rats released 744 ± 260 and 1578 ± 630 nmoles/10 min at 8 and 12 weeks of age, respectively. Perfusion with insulin increased FA release by 32%. Thus in vitro and ex vivo findings suggest that nonadipose tissues such as myocardium can export FA when the unoxidized lipid content is excessive.


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