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J. Lipid Res.
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Originally published In Press as doi:10.1194/jlr.R800085-JLR200 on November 24, 2008

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Journal of Lipid Research, Vol. 50, S86-S90, April 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology

Metabolism

Regulation of fatty acid uptake into tissues: lipoprotein lipase- and CD36-mediated pathways

Ira J. Goldberg1,*, Robert H. Eckel{dagger} and Nada A. Abumrad§

* Division of Preventive Medicine and Nutrition, Department of Medicine, Columbia University, New York, NY
{dagger} Division of Endocrinology, Diabetes, and Metabolism, University of Colorado at Denver, Aurora, CO
§ Department of Medicine, Center for Human Nutrition, Washington University School of Medicine, St. Louis, MO

Published, JLR Papers in Press, November 24, 2008.

1 To whom correspondence should be addressed. e-mail: iijg3{at}columbia.edu


ABSTRACT

Cells obtain FAs either from LPL-catalyzed hydrolysis of lipoprotein triglyceride or from unesterified FFAs associated with albumin. LPL also influences uptake of esterified lipids such as cholesteryl and retinyl esters that are not hydrolyzed in the plasma. This process might not involve LPL enzymatic activity. LPL is regulated by feeding/fasting, insulin, and exercise. Although a number of molecules may affect cellular uptake of FFAs, the best characterized is CD36. Genetic deletion of this multiligand receptor reduces FFA uptake into skeletal muscle, heart, and adipose tissue, and impairs intestinal chylomicron production and clearance of lipoproteins from the blood. CD36 is regulated by some of the same factors that regulate LPL, including insulin, muscle contraction, and fasting, in part, via ubiquitination. LPL and CD36 actions in various tissues coordinate biodistribution of fat-derived calories.

Supplementary key words lipase • fatty acids • CD36 • insulin actions • triglyceride


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JLR 50th Anniversary Collections
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