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

M Pravenec; V Landa; V Zidek; A Musilova; V Kren; L Kazdova; T J Aitman; A M Glazier; A Ibrahimi; N A Abumrad; N Qi; J M Wang; E M St  Lezin; T W Kurtz

doi:10.1038/84777

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

Nat Genet. 2001 Feb;27(2):156-8. doi: 10.1038/84777.

Authors

M Pravenec¹, V Landa, V Zidek, A Musilova, V Kren, L Kazdova, T J Aitman, A M Glazier, A Ibrahimi, N A Abumrad, N Qi, J M Wang, E M St Lezin, T W Kurtz

Affiliation

¹ Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.

PMID: 11175782
DOI: 10.1038/84777

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.

Publication types

Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

MeSH terms

Animals
Animals, Genetically Modified
CD36 Antigens / biosynthesis
CD36 Antigens / genetics*
Fatty Acids / blood
Glucose Tolerance Test
Hypertension / genetics*
Insulin Resistance / genetics*
Rats
Rats, Inbred SHR

Substances

CD36 Antigens
Fatty Acids

Abstract

Publication types

MeSH terms

Substances

Grants and funding