Role of FAT/CD36 in novel PKC isoform activation in heart of spontaneously hypertensive rats
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
- MeSH
- aktivace enzymů MeSH
- antigeny CD36 genetika metabolismus MeSH
- cytosol metabolismus MeSH
- inzulin krev metabolismus MeSH
- inzulinová rezistence genetika fyziologie MeSH
- krevní glukóza analýza metabolismus MeSH
- krysa rodu Rattus MeSH
- kyseliny mastné neesterifikované krev metabolismus MeSH
- myokard metabolismus MeSH
- potkani inbrední SHR MeSH
- proteinkinasa C-delta biosyntéza MeSH
- proteinkinasa C-epsilon biosyntéza MeSH
- regulace genové exprese MeSH
- sacharosa metabolismus MeSH
- signální transdukce MeSH
- srdeční komory metabolismus MeSH
- triglyceridy krev metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- antigeny CD36 MeSH
- inzulin MeSH
- krevní glukóza MeSH
- kyseliny mastné neesterifikované MeSH
- proteinkinasa C-delta MeSH
- proteinkinasa C-epsilon MeSH
- sacharosa MeSH
- triglyceridy MeSH
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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