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Submitted on August 26, 2004
Accepted on January 17, 2005
Institutes of Physiology and Clinical Medicine, National Yang-Ming University, and Department of Medical Research & Education, Taipei Veterans General Hospital, Taipei, Taiwan
* To whom correspondence should be addressed. E-mail: ltho{at}vghtpe.gov.tw.
The renin-angiotensin system (RAS) plays a critical role in the pathogenesis of obesity, obesity-associated hypertension, and insulin resistance. However, the biological actions of angiotensin II (AII) on insulin sensitivity remain controversial. Since angiotensinogen and AII receptors are expressed on adipose tissue, we investigated the effect of AII on the insulin sensitivity of isolated rat adipocytes. Results of receptor binding assay showed the maximal AII binding capacity of adipocytes to be 8.3 ± 0.9 fmol / 7x106cells and the dissociation constant 2.72 ± 0.11 nM. Substantial expression of both types 1 and 2 AII (AT1 and AT2) receptors was detected using the RT PCR. AII had no effect on basal glucose uptake, but significantly potentiated insulin-stimulated glucose uptake, this effect being abolished by AT1 antagonist, losartan. In addition, AII did not alter the insulin binding capacity of adipocytes, but increased insulin-stimulated tyrosine phosphorylation of the insulin receptor 
subunit, Akt phosphorylation, and translocation of GLUT4 to the plasma membrane. AII potentiated insulin-stimulated glucose uptake through the AT1 receptor and by alteration of the intracellular signaling of insulin. Intraperitoneal injection of Sprague Dawley rats with AII increased insulin sensitivity in vivo. In conclusion, we have shown that AII enhances insulin sensitivity both in vitro and in vivo, suggesting that dysregulation of the insulin-sensitizing effect of AII may be involved in the development of insulin resistance.
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