Dynamic role of the transmembrane glycoprotein CD36 (SR-B2) in cellular fatty acid uptake and utilization

The widely expressed transmembrane glycoprotein, cluster of differentiation 36 (CD36), a scavenger receptor class B protein (SR-B2), serves many functions in lipid metabolism and signaling. Here, we review CD36's role in facilitating cellular long-chain fatty acid uptake across the plasma membr...

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Bibliographic Details
Published in:Journal of lipid research 2018, Vol.59 (7), p.1084-1093
Main Authors: Glatz, JanF.C., Luiken, JoostJ.F.P.
Format: Article
Language:English
Subjects:
Animals
Biological Transport
Cardiomyopathy
CD36 antigen
CD36 Antigens - chemistry
CD36 Antigens - metabolism
Cell surface
cluster of differentiation 36
Diabetes mellitus
Endosomes
Fatty acid-binding protein
Fatty acids
Fatty Acids - metabolism
Glycoproteins
heart
High fat diet
Homeostasis
Humans
Insulin
Insulin Resistance
Lipid metabolism
Lipids
Membrane proteins
Metabolism
muscle
Muscles - metabolism
Myocytes
Protein turnover
Proteins
scavenger receptor B2
Scavenger receptors
Skeletal muscle
Thematic Review Series
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Summary:The widely expressed transmembrane glycoprotein, cluster of differentiation 36 (CD36), a scavenger receptor class B protein (SR-B2), serves many functions in lipid metabolism and signaling. Here, we review CD36's role in facilitating cellular long-chain fatty acid uptake across the plasma membrane, particularly in heart and skeletal muscles. CD36 acts in concert with other membrane proteins, such as peripheral plasma membrane fatty acid-binding protein, and is an intracellular docking site for cytoplasmic fatty acid-binding protein. The cellular fatty-acid uptake rate is governed primarily by the presence of CD36 at the cell surface, which is regulated by the subcellular vesicular recycling of CD36 from endosomes to the plasma membrane. CD36 has been implicated in dysregulated fatty acid and lipid metabolism in pathophysiological conditions, particularly in high-fat diet-induced insulin resistance and diabetic cardiomyopathy. Current research is exploring signaling pathways and vesicular trafficking routes involving CD36 to identify metabolic targets to manipulate the cellular utilization of fatty acids. Because of its rate-controlling function in the use of fatty acids in the heart and muscle, CD36 would be a preferable target to protect myocytes against lipotoxicity. Despite a poor understanding of its mechanism of action, CD36 has emerged as a pivotal membrane protein involved in whole-body lipid homeostasis.
ISSN:0022-2275
1539-7262
1539-7262
DOI:10.1194/jlr.R082933