Fatty acid transport in skeletal muscle: role in energy provision and insulin resistance

Graham P. Holloway, Robert W. Schwenk, Joost J. F. P. Luiken, Jan F. C. Glatz, Arend Bonen*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

6 Citations (Web of Science)

Abstract

Long-chain fatty acid uptake has now been shown to occur via a highly regulated, protein-mediated mechanism involving plasma membrane fatty acid transporters. This process is especially important in skeletal muscle, a tissue with a highly variable metabolic rate that constitutes approximately 40% of body mass. We review the evidence that skeletal muscle fatty acid transport is acutely and chronically regulated by muscle contraction and insulin, largely by the fatty acid transporter CD36. We also examine recent data suggesting that CD36 may contribute to regulating fatty acid oxidation by mitochondria. In addition, we review evidence showing that skeletal muscle insulin resistance is associated with the dysregulation of CD36-mediated fatty acid transport, and that the insulin-sensitizing effects of proliferator-activated receptor-gamma coactivator-I alpha may depend on limiting CD36 upregulation. Taken altogether, it is apparent that skeletal muscle fatty acid transport is central to the regulation of whole-body lipid metabolism in health and disease.
Original languageEnglish
Pages (from-to)731-745
JournalClinical Lipidology
Volume5
Issue number5
DOIs
Publication statusPublished - Oct 2010

Keywords

  • CD36
  • exercise training
  • FATPI
  • FATP4
  • GLUT4
  • insulin
  • insulin resistance
  • muscle contraction
  • plasma membrane-associated FABP
  • proliferator-activated receptor-gamma coactivator-I alpha

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