Does Cd36 gene play a key role in disturbed glucose and fatty acid metabolism in Prague hypertensive hypertriglyceridemic rats?
Jazyk angličtina Země Česko Médium print
Typ dokumentu srovnávací studie, časopisecké články, práce podpořená grantem
PubMed
15209533
Knihovny.cz E-zdroje
- MeSH
- antigeny CD36 genetika metabolismus MeSH
- fylogeneze MeSH
- glukosa metabolismus MeSH
- hypertenze genetika metabolismus MeSH
- hypertriglyceridemie genetika metabolismus MeSH
- inzulinová rezistence genetika MeSH
- krysa rodu Rattus MeSH
- lidé MeSH
- mastné kyseliny metabolismus MeSH
- metabolický syndrom genetika metabolismus MeSH
- modely nemocí na zvířatech MeSH
- polymorfismus genetický MeSH
- potkani inbrední LEW MeSH
- potkani inbrední WKY MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- lidé MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
- Názvy látek
- antigeny CD36 MeSH
- glukosa MeSH
- mastné kyseliny MeSH
Close links between hypertension, hypertriglyceridemia, insulin resistance and other symptoms of metabolic syndrome was demonstrated in humans and experimental animals. Quantitative trait loci for defects in glucose and fatty acid metabolism, hypertriglyceridemia and hypertension were mapped in spontaneously hypertensive rats (SHR) on chromosome 4 and defective Cd36 gene was identified in this region. Here we investigated the polymorphism of Cd36 gene in Prague hereditary hypertriglyceridemic (HTG) rats, which represent another model of genetic hypertension and metabolic syndrome. These animals were compared with NIH-derived SHR and two different normotensive control strains (WKY, LEW). In spite of the fact that HTG and SHR rats had similar metabolic disturbances, genotype analysis of PCR products has shown that Cd36 mutation was not present in HTG rats. In conclusion, we have revealed that defective Cd36 is probably a candidate gene for disorded fatty-acid metabolism, glucose intolerance and insulin resistance in NIH-derived SHR, but other genes might play a role in pathogenesis of metabolic syndrome in Prague hereditary hypertriglyceridemic rats. This is in accordance with the absence of defective Cd36 gene in original SHR from Japan.
Research on Experimental Hypertension in Prague (1966-2009)