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

被引：0
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作者：
Michal Pravenec
Vladimir Landa
Vaclav Zidek
Alena Musilova
Vladimir Kren
Ludmila Kazdova
Timothy J. Aitman
Anne M. Glazier
Azeddine Ibrahimi
Nada A. Abumrad
Nianning Qi
Jia-Ming Wang
Elizabeth M. St. Lezin
Theodore W. Kurtz
机构：
[1] Institutes of Physiology,MRC Clinical Sciences Centre and Division of National Heart & Lung Institute
[2] Czech Academy of Sciences,Department of Physiology and Biophysics
[3] Molecular Genetics,Department of Laboratory Medicine
[4] Czech Academy of Sciences,undefined
[5] Institute of Biology and Medical Genetics,undefined
[6] 1st Medical Faculty,undefined
[7] Charles University,undefined
[8] Institute for Clinical and Experimental Medicine,undefined
[9] Molecular Medicine Group,undefined
[10] Imperial College School of Medicine,undefined
[11] Hammersmith Hospital,undefined
[12] State University of New York,undefined
[13] University of California,undefined
来源：
Nature Genetics | 2001年 / 27卷
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摘要：
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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页码：156 / 158
页数：2
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