Regulation of fatty acid uptake into tissues: Lipoprotein lipase- And CD36-mediated pathways

Ira J. Goldberg, Robert H. Eckel, Nada A. Abumrad

Research output: Contribution to journalReview articlepeer-review

271 Scopus citations

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.

Original languageEnglish
Pages (from-to)S86-S90
JournalJournal of lipid research
Volume50
Issue numberSUPPL.
DOIs
StatePublished - Apr 2009

Keywords

  • CD36
  • Fatty acids
  • Insulin actions
  • Lipase
  • Triglyceride

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