Role of FAT/CD36 in novel PKC isoform activation in heart of spontaneously hypertensive rats
作者： Martina J. Klevstig , Irena Markova , Jana Burianova , Ludmila Kazdova , Michal Pravenec
DOI: 10.1007/S11010-011-0886-2
关键词:
摘要: Disruption to the sensitive balance of long-chain fatty acids and glucose in heart could cause cardiovascular diseases. Searching for a possible role novel protein kinase C (nPKC) with disrupted energy balance, we compared insulin-resistant spontaneously hypertensive rats (SHR), which carry nonfunctional variant acid transporter FAT/CD36, less congenic strain SHR-4 that is genetically identical except segment on chromosome 4 including wild-type gene functional FAT/CD36. We analyzed expression nPKC-δ -e isoforms plus triacylglycerols (TAG) content myocardium both FAT/CD36 strains after high sucrose diet (HSD). Two weeks before killing, males were randomly divided into two groups fed either standard laboratory chow or an HSD. PKC was determined by Western blotting particulate cytosolic fractions from left ventricles. The exhibited lower serum levels insulin free than did SHR higher amounts PKC-e fraction. HSD caused accumulation TAG but not SHR-4. increased PKC-δ decreased fraction ventricles while having no effects SHR. These results demonstrate reduced resistance associated signaling pathway involving nPKCs.
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