Cellular fatty acid uptake: a pathway under construction

Trends Endocrinol Metab. 2009 Mar;20(2):72-7. doi: 10.1016/j.tem.2008.11.001. Epub 2009 Jan 29.


Membrane uptake of long-chain fatty acids (FAs) is the first step in cellular FA utilization and a point of metabolic regulation. CD36 facilitates a major fraction of FA uptake by key tissues. This review highlights the contribution of CD36 to pathophysiology in rodents and humans. Novel concepts regarding regulation of CD36-facilitated uptake are discussed (i.e. the role of membrane rafts and caveolae, CD36 recycling between intracellular depots and the membrane, and chemical modifications of the protein that impact its turnover and recruitment). Importantly, CD36 membrane levels and turnover are abnormal in diabetes, resulting in dysfunctional FA utilization. In addition, variants in the CD36 gene were shown recently to influence susceptibility for the metabolic syndrome, which greatly increases the risk of diabetes and heart disease.

Publication types

  • Review

MeSH terms

  • Animals
  • CD36 Antigens / genetics
  • CD36 Antigens / metabolism
  • CD36 Antigens / physiology
  • Fatty Acid Transport Proteins / metabolism
  • Fatty Acid Transport Proteins / physiology
  • Fatty Acids / metabolism*
  • Genetic Predisposition to Disease
  • Humans
  • Metabolic Diseases / genetics
  • Metabolic Diseases / metabolism
  • Metabolic Networks and Pathways / genetics
  • Metabolic Networks and Pathways / physiology*
  • Models, Biological
  • Protein Transport / physiology
  • Rodentia / genetics
  • Rodentia / metabolism
  • Ubiquitination / physiology


  • CD36 Antigens
  • Fatty Acid Transport Proteins
  • Fatty Acids