Transgenic expression of CD36 in the spontaneously hypertensive rat is associated with amelioration of metabolic disturbances but has no effect on hypertension

被引:48
作者
Pravenec, M [1 ]
Landa, V
Zídek, V
Musilová, A
Kazdová, L
Qi, N
Wang, J
St Lezin, E
Kurtz, TW
机构
[1] Acad Sci Czech Republ, Inst Physiol, Videnska 1083, CR-14220 Prague 4, Czech Republic
[2] Ctr Integrated Genom, Prague, Czech Republic
[3] Charles Univ Prague, Fac Med 1, Inst Biol & Med Genet, Prague, Czech Republic
[4] Inst Clin & Expt Med, Prague, Czech Republic
[5] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA
[6] Dept Vet Affairs Med Ctr, San Francisco, CA USA
关键词
SHR; Cd36; transgenic animal; blood pressure; insulin resistance; fatty acids;
D O I
10.33549/physiolres.930380
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Spontaneously hypertensive rats (SHR/NIH strain) harbor a deletion variant in the Cd36 fatty acid transporter and display defective fatty acid metabolism, insulin resistance and hypertension. Transgenic rescue of Cd36 in SHR ameliorates insulin resistance and improves dyslipidemia. However, the role of Cd36 in blood pressure regulation remains controversial due to inconsistent blood pressure effects that were observed with transgenic expression of Cd36 on the SHR background. In the current studies, we developed two new SHR transgenic lines, which express wild type Cd36 under the control of the universal Ef-1alpha promoter, and examined the effects of transgenic expression of wild type Cd36 on selected metabolic and cardiovascular phenotypes. Transgenic expression of Cd36 in the new lines was associated with significantly decreased serum fatty acids, amelioration of insulin resistance and glucose intolerance but failed to induce any consistent changes in blood pressure as measured by radiotelemetry. The current findings confirm the genetic association of defective Cd36 with disordered insulin action and fatty acid metabolism in the SHR/NIH strain and suggest that Cd36 is linked to other gene(s) on rat chromosome 4 that regulate blood pressure.
引用
收藏
页码:681 / 688
页数:8
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