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

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 pro...

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Veröffentlicht in:Nature genetics 2001-02, Vol.27 (2), p.156-158
Hauptverfasser: Pravenec, Michal, Landa, Vladimir, Zidek, Vaclav, Musilova, Alena, Kren, Vladimir, Kazdova, Ludmila, Aitman, Timothy J., Glazier, Anne M., Ibrahimi, Azeddine, Abumrad, Nada A., Qi, Nianning, Wang, Jia-Ming, St. Lezin, Elizabeth M., Kurtz, Theodore W.
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container_end_page 158
container_issue 2
container_start_page 156
container_title Nature genetics
container_volume 27
creator Pravenec, Michal
Landa, Vladimir
Zidek, Vaclav
Musilova, Alena
Kren, Vladimir
Kazdova, Ludmila
Aitman, Timothy J.
Glazier, Anne M.
Ibrahimi, Azeddine
Abumrad, Nada A.
Qi, Nianning
Wang, Jia-Ming
St. Lezin, Elizabeth M.
Kurtz, Theodore W.
description 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.
doi_str_mv 10.1038/84777
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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. 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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. 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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.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>11175782</pmid><doi>10.1038/84777</doi><tpages>3</tpages></addata></record>
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subjects Agriculture
Animal Genetics and Genomics
Animals
Animals, Genetically Modified
Biological and medical sciences
Biomedical and Life Sciences
Biomedicine
brief-communication
Cancer Research
Care and treatment
CD36 Antigens - biosynthesis
CD36 Antigens - genetics
Cd36 gene
Cell metabolism, cell oxidation
Cell physiology
Diagnosis
Fatty acids
Fatty Acids - blood
Fundamental and applied biological sciences. Psychology
Gene Function
Genetic aspects
Genetic testing
Genetics
Glucose Tolerance Test
Hominids
Human Genetics
Hypertension
Hypertension - genetics
Identification and classification
Insulin resistance
Insulin Resistance - genetics
Metabolism
Mitochondrial DNA
Molecular and cellular biology
Monkeys & apes
Multifactorial traits
Physiological aspects
Population
Publishing
Rats
Rats, Inbred SHR
Research centers
Risk factors
title Transgenic rescue of defective Cd36 ameliorates insulin resistance in spontaneously hypertensive rats
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