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Experimental Diabetes Research
Volume 2011, Article ID 947138, 7 pages
Research Article

Electroacupuncture-Induced Cholinergic Nerve Activation Enhances the Hypoglycemic Effect of Exogenous Insulin in a Rat Model of Streptozotocin-Induced Diabetes

1Department of Acupuncture, China Medical University Hospital, Taichung, Taiwan
2School of Chinese Medicine, China Medical University, Taichung, Taiwan
3College of Life Sciences, National Tsing Hua University, Hsinchu, Taiwan
4Department of Orthopedics, Taichung Veterans General Hospital, Taichung, Taiwan
5Department of Internal Medicine, Lee's General Hospital, Miaoli, Taiwan
6Department of Medicinal Botanicals and Health Care, Da-Yeh University, Chunghwa, Taiwan
7College of Life Sciences, National Chung Hsing University, Taichung, Taiwan

Received 19 February 2011; Revised 24 March 2011; Accepted 28 April 2011

Academic Editor: Mark A. Yorek

Copyright © 2011 Yu-Chen Lee et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The aim of this study is to explore the mechanisms by which electroacupuncture (EA) enhances the hypoglycemic effect of exogenous insulin in a streptozotocin- (STZ-) diabetic rats. Animals in the EA group were anesthetized and subjected to the insulin challenge test (ICT) and EA for 60 minutes. In the control group, rats were subjected to the same treatment with the exception of EA stimulation. Blood samples were drawn to measure changes in plasma glucose, free fatty acids (FFA), and insulin levels. Western blot was used to assay proteins involved in insulin signaling. Furthermore, atropine, hemicholinium-3 (HC-3), and Eserine were used to explore the relationship between EA and cholinergic nerve activation during ICT. EA augmented the blood glucose-lowering effects of EA by activating the cholinergic nerves in STZ rats that had been exposed to exogenous insulin. This phenomenon may be related to enhancement of insulin signaling rather than to changes in FFA concentration.