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

Publikace na Přírodovědecká fakulta, Ústřední knihovna |
2011

Tento text není v aktuálním jazyce dostupný. Zobrazuje se verze "en".Abstrakt

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. Our results demonstrate that reduced insulin resistance in SHR-4 rats is associated with the insulin signaling pathway involving nPKCs.