Changes in the activity of some metabolic enzymes in the heart of SHR rat incurred by transgenic expression of CD36
Language English Country Spain Media print-electronic
Document type Journal Article
Grant support
1016214
Grantová Agentura, Univerzita Karlova
14-36804
Grantová Agentura České Republiky
SVV-260434/2018
Univerzita Karlova v Praze
PubMed
29916179
DOI
10.1007/s13105-018-0641-1
PII: 10.1007/s13105-018-0641-1
Knihovny.cz E-resources
- Keywords
- CD36, Heart, Left and right ventricles, Mitochondria, OXPHOS, SHR,
- MeSH
- ATP-Binding Cassette Transporters genetics metabolism MeSH
- CD36 Antigens genetics metabolism MeSH
- Gene Expression MeSH
- Hexokinase genetics metabolism MeSH
- Hypertension enzymology genetics physiopathology MeSH
- Insulin Resistance MeSH
- Myocytes, Cardiac enzymology pathology MeSH
- Rats MeSH
- Malate Dehydrogenase genetics metabolism MeSH
- Mitochondria enzymology pathology MeSH
- Oxidative Phosphorylation MeSH
- Rats, Inbred SHR MeSH
- Rats, Transgenic MeSH
- Primary Cell Culture MeSH
- Gene Expression Regulation MeSH
- Oxygen Consumption genetics MeSH
- Heart Ventricles enzymology pathology MeSH
- Succinate Dehydrogenase genetics metabolism MeSH
- Transgenes * MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- ATP-Binding Cassette Transporters MeSH
- Abcd3 protein, rat MeSH Browser
- CD36 Antigens MeSH
- Hexokinase MeSH
- Malate Dehydrogenase MeSH
- Succinate Dehydrogenase 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
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