Abstract
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.
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This work was supported by the GAUK grant no. 1016214 from the Charles University Grant Agency, and by the institutional research projects no. 67985823 (Institute of Physiology, CAS) and SVV-260434/2018 (Charles University in Prague). MP was supported by grant 14-36804 from the Czech Science Foundation.
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Animal experiments were performed in accordance with the Animal Protection Welfare Law of the Czech Republic (311/1997) and were approved by the Ethics Committee of the Institute of Physiology of the Academy of Sciences of the Czech Republic.
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Manakov, D., Kolar, D., Zurmanova, J. et al. Changes in the activity of some metabolic enzymes in the heart of SHR rat incurred by transgenic expression of CD36. J Physiol Biochem 74, 479–489 (2018). https://doi.org/10.1007/s13105-018-0641-1
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DOI: https://doi.org/10.1007/s13105-018-0641-1