Hypertension,
dyslipidemia, and
insulin resistance in the
spontaneously hypertensive rat (SHR) can be alleviated by rescuing CD36
fatty acid translocase. The present study investigated whether transgenic rescue of CD36 in SHR could
affect mitochondrial function and activity of selected metabolic
enzymes in the
heart. These analyses were conducted on ventricular preparations derived from SHR and from transgenic
strain SHR-Cd36 that expresses a functional wild-type CD36. Our respirometric measurements revealed that
mitochondria isolated from the
left ventricles exhibited two times higher respiratory activity than those isolated from the
right ventricles. Whereas, we did not observe any significant changes in functioning of the mitochondrial
respiratory system between both
rat strains,
enzyme activities of total
hexokinase, and both mitochondrial and total
malate dehydrogenase were markedly decreased in the
left ventricles of
transgenic rats, compared to SHR. We also detected downregulated expression of the
succinate dehydrogenase subunit SdhB (complex II) and 70 kDa peroxisomal
membrane protein in the
left ventricles of SHR-Cd36. These data indicate that CD36 may
affect in a unique fashion metabolic substrate
flexibility of the left and
right ventricles