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Brief Communication
Nature Genetics  27, 156 - 158 (2001)
doi:10.1038/84777

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

Michal Pravenec1, 3, Vladimir Landa2, Vaclav Zidek1, Alena Musilova1, Vladimir Kren1, 3, Ludmila Kazdova4, Timothy J. Aitman5, Anne M. Glazier5, Azeddine Ibrahimi6, Nada A. Abumrad6, Nianning Qi7, Jia-Ming Wang7, Elizabeth M. St. Lezin7 & Theodore W. Kurtz7

1  Institutes of Physiology, Czech Academy of Sciences, Prague, Czech Republic.

2  Molecular Genetics, Czech Academy of Sciences, Prague, Czech Republic.

3  Institute of Biology and Medical Genetics, 1st Medical Faculty, Charles University, Prague, Czech Republic.

4  Institute for Clinical and Experimental Medicine, Prague, Czech Republic.

5  Molecular Medicine Group, MRC Clinical Sciences Centre and Division of National Heart & Lung Institute, Imperial College School of Medicine, Hammersmith Hospital, London, UK.

6  Department of Physiology and Biophysics, State University of New York, Stony Brook, New York, USA.

7  Department of Laboratory Medicine, University of California, San Francisco, California, USA.

Correspondence should be addressed to Theodore W. Kurtz KurtzT@Labmed2.ucsf.edu
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.


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Nature Genetics
ISSN: 1061-4036
EISSN: 1546-1718
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