Original Article
International Journal of Obesity (2007) 31, 72–77. doi:10.1038/sj.ijo.0803364; published online 9 May 2006
Altered insulin-mediated and insulin-like growth factor-1-mediated vasorelaxation in aortas of obese Zucker rats
A-L Yang1, J-I Chao1 and S-D Lee2,3
- 1Department of Physical Therapy, College of Medicine, National Cheng Kung University, Tainan, Taiwan
- 2School of Physical Therapy, College of Medical Sciences, Chung Shan Medical University, Taichung, Taiwan
- 3School of Physical Therapy, China Medical University, Taichung, Taiwan
Correspondence: Professor S-D Lee, School of Physical Therapy, China Medical University, 91 Hsueh-Shih Rd, Taichung 40202, Taiwan. E-mail: shinda@csmu.edu.tw
Received 18 November 2005; Revised 14 March 2006; Accepted 15 March 2006; Published online 9 May 2006.
Abstract
Objective:
Insulin and insulin-like growth factor-1 (IGF-1) have vasorelaxant effects in vivo, which is dependent on nitric oxide (NO) production. The aim of this study was to investigate the vasorelaxant responses mediated by insulin and/or IGF-1 in aortas of obese Zucker rats.
Methods:
The thoracic aortas of eight lean and eight obese Zucker rats (6 months old) were isolated for vasorelaxation analysis. Insulin-induced and IGF-1-induced vasorelaxant responses were evaluated by the isometric tension of aortic rings in the organ bathes. The roles of phosphatidylinositol 3-kinase (PI3K) and nitric oxide synthase (NOS) in vasorelaxant responses were examined by treating selective inhibitors, such as wortmannin (an inhibitor of PI3K) and N
-nitro-L-arginine methyl ester (L-NAME, a NOS inhibitor). In addition, the vascular responses to sodium nitroprusside (SNP), a direct vasodilator of vascular smooth muscle, were examined.
Results:
The insulin-induced vasorelaxation in aortas of obese rats was significantly decreased, whereas the IGF-1-induced vasorelaxation was significantly increased, compared with that in lean rats. After the pre-administration of wortmannin or L-NAME, the altered insulin-induced or IGF-1-induced vasorelaxation was abolished. There was no significant difference in the SNP-induced vasorelaxation between lean and obese rats.
Conclusion:
Our findings suggested that the decreased insulin-mediated vasorelaxation in obese rats appeared to be counteracted by the increased IGF-1-mediated vasorelaxation. Furthermore, the NO-dependent pathway was involved in the altered vasorelaxant responses. However, the SNP-induced vasorelaxation was not changed in obese rats.
Keywords:
insulin, IGF-1, phosphatidylinositol 3-kinase, nitric oxide, vasodilation
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