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Changes in the activity of some metabolic enzymes in the heart of SHR rat incurred by transgenic expression of CD36
D. Manakov, D. Kolar, J. Zurmanova, M. Pravenec, J. Novotny,
Jazyk angličtina Země Španělsko
Typ dokumentu časopisecké články
- MeSH
- ABC transportéry genetika metabolismus MeSH
- antigeny CD36 genetika metabolismus MeSH
- exprese genu MeSH
- hexokinasa genetika metabolismus MeSH
- hypertenze enzymologie genetika patofyziologie MeSH
- inzulinová rezistence MeSH
- kardiomyocyty enzymologie patologie MeSH
- krysa rodu rattus MeSH
- malátdehydrogenasa genetika metabolismus MeSH
- mitochondrie enzymologie patologie MeSH
- oxidativní fosforylace MeSH
- potkani inbrední SHR MeSH
- potkani transgenní MeSH
- primární buněčná kultura MeSH
- regulace genové exprese MeSH
- spotřeba kyslíku genetika MeSH
- srdeční komory enzymologie patologie MeSH
- sukcinátdehydrogenasa genetika metabolismus MeSH
- transgeny * MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
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.
Department of Physiology Faculty of Science Charles University Prague Czech Republic
Institute of Physiology of the Czech Academy of Sciences Prague Czech Republic
Citace poskytuje Crossref.org
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- $a 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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