Transgenic rescue of defective Cd36 ameliorates insulin resistance in spontaneously hypertensive rats
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem, Research Support, U.S. Gov't, P.H.S.
Grantová podpora
P01 HL35018
NHLBI NIH HHS - United States
R01 HL56028
NHLBI NIH HHS - United States
R01 HL63709
NHLBI NIH HHS - United States
PubMed
11175782
DOI
10.1038/84777
Knihovny.cz E-zdroje
- MeSH
- antigeny CD36 biosyntéza genetika MeSH
- geneticky modifikovaná zvířata MeSH
- glukózový toleranční test MeSH
- hypertenze genetika MeSH
- inzulinová rezistence genetika MeSH
- krysa rodu Rattus MeSH
- mastné kyseliny krev MeSH
- potkani inbrední SHR MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, U.S. Gov't, P.H.S. MeSH
- Názvy látek
- antigeny CD36 MeSH
- mastné kyseliny MeSH
Spontaneously hypertensive rats (SHR) display several features of the human insulin-resistance syndromes. Cd36 deficiency is genetically linked to insulin resistance in SHR. We show that transgenic expression of Cd36 in SHR ameliorates insulin resistance and lowers serum fatty acids. Our results provide direct evidence that Cd36 deficiency can promote defective insulin action and disordered fatty-acid metabolism in spontaneous hypertension.
Citace poskytuje Crossref.org
Research on Experimental Hypertension in Prague (1966-2009)
Systems genetic analysis of brown adipose tissue function
Translational regulation shapes the molecular landscape of complex disease phenotypes
Role of FAT/CD36 in novel PKC isoform activation in heart of spontaneously hypertensive rats
Recent advances in genetics of the spontaneously hypertensive rat
