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

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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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Figure 1: Transgenic expression of wild-type Cd36 in SHR.
Figure 2: Metabolic effects of expressing wild-type Cd36 on the SHR genetic background.

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Acknowledgements

This work was supported by grants 301/00/1636 and 204/98/K015 from the Grant Agency of the Czech Republic to V.Z. and M.P.; grant LN00A079 from the Ministry of Education of the Czech Republic to M.P.; NIH grants RO1 HL56028 and PO1 HL35018 (project 2) to T.W.K. and RO1 HL63709 to E.M.St.L.; and grant 4904-3 from the Internal Grant Agency of the Ministry of Health of the Czech Republic to L.K. T.J.A. was supported by intramural funding from the MRC Clinical Sciences Center and A.M.G. was supported by an MRC Studentship (G78/5347). M.P. is an International Research Scholar of the Howard Hughes Medical Institute and E.M.St.L. is a recipient of a Mentored Clinical Scientist Award from the NIH/NHLBI.

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Correspondence to Theodore W. Kurtz.

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Pravenec, M., Landa, V., Zidek, V. et al. Transgenic rescue of defective Cd36 ameliorates insulin resistance in spontaneously hypertensive rats. Nat Genet 27, 156–158 (2001). https://doi.org/10.1038/84777

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