Transgenic rescue of defective Cd36 ameliorates insulin resistance in spontaneously hypertensive rats
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.
Grant support
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-resources
- MeSH
- CD36 Antigens biosynthesis genetics MeSH
- Animals, Genetically Modified MeSH
- Glucose Tolerance Test MeSH
- Hypertension genetics MeSH
- Insulin Resistance genetics MeSH
- Rats MeSH
- Fatty Acids blood MeSH
- Rats, Inbred SHR MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, U.S. Gov't, P.H.S. MeSH
- Names of Substances
- CD36 Antigens MeSH
- Fatty Acids 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.
References provided by 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
