Heart mitochondrial fatty acid oxidation is not affected by deletion of the fatty acid transporter CD36/FAT

Background and objective Plasma membrane CD36/FAT is involved in uptake of fatty acids. The protein also has been recently localized to mitochondria in heart and skeletal muscle and reported to facilitate mitochondrial oxidation of fatty acids. The goal of the study was to determine the site of CD36/FAT effect on mitochondrial fatty acid oxidation. Approach and methods. We isolated heart subsarcolemmal and interfibrillar mitochondria from wild type and CD36 knockout mice and determined the following parameters: (a) Oxidative phosphorylation with the non‐lipid substrate pyruvate/malate, and with palmitate, palmitoyl‐CoA, and palmitoylcarnitine as lipid substrates; (b) The activities of long‐chain acyl‐CoA synthase and carnitine palmitoyltransferase 1 (CPT1b) as well the sensitivity of CPT1b to inhibition by malonyl‐CoA; (c) Oxidation of isotope‐labeled oleic and palmitic acid in whole heart homogenates; and (d) Activities of respiratory chain enzymes. Results Compared to wild type, there was a trend in all measured parameters to be increased by ablation of CD36/FAT, however, the increase did not reach statistical significance. These results extend and are consistent with data previously published by us. Conclusion The data from our study provide evidence against the involvement of CD36/FAT in mitochondrial fatty acid oxidation at any step of the overall pathway. Supported by PO1 AG15885