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

被引：0

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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D O I：

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学科分类号：

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.

引用

页码：156 / 158

页数：2

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