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eCAM Advance Access originally published online on July 28, 2004
eCAM 2004 1(2):193-201; doi:10.1093/ecam/neh027
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© 2004, the authors Evidenced-based Complementary and Alternative Medicine, Vol. 1, Issue 2 © Oxford University Press 2004; all rights reserved. The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated.

Original Article

Mediation of Endogenous ß-endorphin by Tetrandrine to Lower Plasma Glucose in Streptozotocin-induced Diabetic Rats

Jen-Hao Hsu1, Yang-Chang Wu1, Shorong-Shii Liou2, I-Min Liu2, Lee-Wen Huang3 and Juei-Tang Cheng3,*

1Graduate Institute of Natural Products, Kaohsiung Medical University Kaohsiung City, Taiwan, 2Department of Pharmacy, Tajen Institute of Technology Yen-Pou, Ping Tung Shien, Taiwan, and 3Department of Pharmacology, College of Medicine, National Cheng Kung University Tainan City, Taiwan

The role of ß-endorphin in the plasma glucose-lowering action of tetrandrine in streptozotocin-induced diabetic rats (STZ-diabetic rats) was investigated. The plasma glucose concentration was assessed by the glucose oxidase method. The enzyme-linked immunosorbent assay was used to determine the plasma level of ß-endorphin-like immunoreactivity (BER). The mRNA levels of glucose transporter subtype 4 (GLUT4) in soleus muscle and phosphoenolpyruvate carboxykinase (PEPCK) in the liver of STZ-diabetic rats were detected by Northern blotting analysis. The expressed protein of GLUT4 or PEPCK was characterized by Western blotting analysis. Tetrandrine dose-dependently increased plasma BER in a manner parallel to the decrease of plasma glucose in STZ-diabetic rats. Moreover, the plasma glucose-lowering effect of tetrandrine was inhibited by naloxone and naloxonazine at doses sufficient to block opioid µ-receptors. Further, tetrandrine failed to produce plasma glucose-lowering action in opioid µ-receptor knockout diabetic mice. Bilateral adrenalectomy eliminated the plasma glucose-lowering effect and plasma BER-elevating effect of tetrandrine in STZ-diabetic rats. Both effects were abolished by treatment with hexamethonium or pentolinium at doses sufficient to block nicotinic receptors. Tetrandrine enhanced BER release directly from the isolated adrenal medulla of STZ-diabetic rats and this action was abolished by the blockade of nicotinic receptors. Repeated intravenous administration of tetrandrine (1.0 mg/kg) to STZ-diabetic rats for 3 days resulted in an increase in the mRNA and protein levels of the GLUT4 in soleus muscle, in addition to the lowering of plasma glucose. Similar treatment with tetrandrine reversed the elevated mRNA and protein levels of PEPCK in the liver of STZ-diabetic rats. The obtained results suggest that tetrandrine may induce the activation of nicotinic receptors in adrenal medulla to enhance the secretion of ß-endorphin, which could stimulate opioid µ-receptors to increase glucose utilization or/and reduce hepatic gluconeogenesis to lower plasma glucose levels in STZ-diabetic rats.

Keywords: tetrandrine – opioid µ-receptors – ß-endorphin – nicotinic receptors – glucose transporters subtype 4 – phosphoenolpyruvate carboxykinase

*For reprints and all correspondence: Juei-Tang Cheng, Tel: +886-6-237-2706; Fax: +886-6-238-6548. E-mail: jtcheng{at}mail.ncku.edu.tw


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