Transgenic rescue of defective Cd36 ameliorates insulin resistance in spontaneously hypertensive rats
M Pravenec, V Landa, V Zidek, A Musilova, V Kren… - Nature …, 2001 - nature.com
M Pravenec, V Landa, V Zidek, A Musilova, V Kren, L Kazdova, TJ Aitman, AM Glazier…
Nature genetics, 2001•nature.comSpontaneously 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.
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.
Abstract
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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