Transgenic rescue of defective Cd36 ameliorates insulin resistance in spontaneously hypertensive rats

0142120 - FGU-C 20010171 RIV US eng J - Journal Article
Pravenec, Michal - Landa, Vladimír - Zídek, Václav - Musilová, Alena - Křen, Vladimír - Kazdová, L. - Aitman, T. J. - Glazier, A. M. - Ibrahimi, A. - Abumrad, N. A. - Qi, N. - Wang, J. M. - St.Lezin, E. M. - Kurtz, W. T.
Transgenic rescue of defective Cd36 ameliorates insulin resistance in spontaneously hypertensive rats.
Nature Genetics. Roč. 27, č. 2 (2001), s. 156-158. ISSN 1061-4036. E-ISSN 1546-1718
R&D Projects: GA ČR GA301/00/1636; GA ČR GV204/98/K015; GA MŠMT LN00A079
Grant - others:HHMI(US) 55000331
Institutional research plan: CEZ:AV0Z5011922
Keywords : Cd36 (fatty acid transporter)
Subject RIV: EB - Genetics ; Molecular Biology
Impact factor: 29.600, year: 2001

We found that in SHR harboring the deletion variant of Cd36 (fatty acid transporter), transgenic expression of wild type Cd36 in modest amounts ameliorates defects in fatty acid metabolism, glucose tolerance, and insulin stimulated glucose uptake in muscle and fat tissue and second, exerts little or no effect on blood pressure. In conclusion, the current studies provide definitive evidence that mutant Cd36 is a QTL with major effect on insulin action, glucose tolerance, and serum fatty acid levels in the SHR/NIH strains.
Permanent Link: http://hdl.handle.net/11104/0039829