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Role of FAT/CD36 in novel PKC isoform activation in heart of spontaneously hypertensive rats

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Abstract

Disruption to the sensitive balance of long-chain fatty acids and glucose in the heart could cause cardiovascular diseases. Searching for a possible role of novel protein kinase C (nPKC) in heart with disrupted energy balance, we compared the insulin-resistant spontaneously hypertensive rats (SHR), which carry a nonfunctional variant of the fatty acid transporter FAT/CD36, with the less insulin-resistant congenic strain SHR-4 that is genetically identical except for a segment on chromosome 4 including a wild-type gene for a functional FAT/CD36. We analyzed expression of the nPKC-δ and -ε isoforms plus triacylglycerols (TAG) content in the myocardium of both FAT/CD36 strains and after a high sucrose diet (HSD). Two weeks before killing, males of both strains were randomly divided into two groups and fed either a standard laboratory chow or an HSD. PKC was determined by Western blotting in particulate and cytosolic fractions from left ventricles. The SHR-4 rats exhibited lower serum levels of insulin and free fatty acids than did SHR rats and higher amounts of PKC-ε in the heart particulate fraction. HSD caused accumulation of heart TAG in SHR but not in SHR-4. HSD increased PKC-δ and decreased PKC-ε expression in particulate fraction from left ventricles of SHR-4 while having no effects in SHR. These results demonstrate that reduced insulin resistance in SHR-4 rats with wild-type FAT/CD36 is associated with the insulin signaling pathway involving nPKCs.

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Acknowledgments

This work was supported by the grants no. 305/08/H037 from the Grant Agency of the Czech Republic, MSM 0021620858 and ME08006 from the Ministry of Education, Youth and Sports of the Czech Republic and by project SVV No. 33779266 from Charles University in Prague.

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Correspondence to Frantisek Novak.

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Klevstig, M.J., Markova, I., Burianova, J. et al. Role of FAT/CD36 in novel PKC isoform activation in heart of spontaneously hypertensive rats. Mol Cell Biochem 357, 163–169 (2011). https://doi.org/10.1007/s11010-011-0886-2

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