Fatty acid oxidation in cardiac and skeletal muscle mitochondria is unaffected by deletion of CD36.
Recent studies found that the plasma membrane fatty acid transport protein CD36 also resides in mitochondrial membranes in cardiac and skeletal muscle. Pharmacological studies suggest that CD36 may play an essential role in mitochondrial fatty acid oxidation. We isolated cardiac and skeletal muscle mitochondria from wild type and CD36 knock-out mice. There were no differences between wild type and CD36 knock-out mice in mitochondrial respiration with palmitoyl-CoA, palmitoyl-carnitine or glutamate as substrate. We investigated a potential alternative role for CD36 in mitochondria, i.e. the export of fatty acids generated in the matrix. Palmitate export was not different between wild type and CD36 knock-out mice. Taken together, CD36 does not appear to play an essential role in mitochondrial uptake of fatty acids or export of fatty acid anions.
King
Kristen L
KL
Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, USA.
Stanley
William C
WC
Rosca
Mariana
M
Kerner
Janos
J
Hoppel
Charles L
CL
Febbraio
Maria
M
D000818:Animals; D018955:CD36 Antigens / Q000235:genetics / Q000378:metabolism*; D002478:Cells, Cultured; D005227:Fatty Acids / Q000378:metabolism*; D017353:Gene Deletion; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D008929:Mitochondria, Heart / Q000378:metabolism*; D008931:Mitochondria, Muscle / Q000378:metabolism*; D010084:Oxidation-Reduction
D018955:CD36 Antigens; D005227:Fatty Acids