CD36 Genotype and Long-Chain Fatty Acid Uptake in the Heart

抄録

Homozygous or compound heterozygous mutation of the CD36 gene (CD36^-/-) in humans results in severe defects of the uptake of long-chain fatty acids (LCFAs) in the heart. Because the effect of a single mutation of this gene (CD36^+/-) on the LCFA uptake is not known, it was evaluated in 29 subjects with the CD36 wild-type gene (WT) (6 healthy subjects, 10 patients with heart disease), CD36^+/- (4 healthy subjects, 5 patients) and CD36^-/- (4 patients). The CD36 genotype was identified in the coding region of genomic DNA, and the expression of CD36 protein was examined by flow cytometry after staining with monoclonal anti-CD36 antibody. The LCFA uptake in the heart was assessed as the radioactivity accumulation ratio of heart to mediastinum after intravenous administration of iodine-123 15-(p-iodophenyl)-3-R, S-methylpentadecanoic acid (H/M ratio). The H/M ratios in WT, CD36^+/- and CD36^-/- were 2.28±0.10, 1.90±0.06 and 1.40±0.11, respectively (p<0.0001, among groups). The H/M ratio between healthy subjects and patients with heart disease for WT and CD36^+/- did not differ significantly (ie, those of WT and CD36^+/- in healthy subjects and patients were 2.29±0.08 vs 2.27±0.12 and 1.90±0.07 vs 1.89±0.05, respectively). Not only CD36^-/- but also CD36^+/- resulted in a significant reduction of the LCFA uptake in the heart independent of heart disease, suggesting genotype dependency and that CD36 might be a fundamental determinant of myocardial LCFA uptake. (Circ J 2002; 66: 819 - 825)