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

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


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


  • CD36 Antigens
  • Fatty Acids