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Journal of Chinese Integrative Medicine ›› 2010, Vol. 8 ›› Issue (6): 535-540.doi: 10.3736/jcim20100605

• Original Experimental Research • Previous Articles     Next Articles

Antidiabetic effects of Tangnaikang on obese Zucker rats and the mechanism

Xiang-yu Guoa,b,Ying Duanc,Juan-e Lia,b,Li-xia Yanga,Lian-sha Huanga,b,Zhi-cheng Wanga,He-yao Wangd,Tong-hua Liua,b   

  1. a Beijing University of Chinese Medicine, Beijing 100029, China
    b Department of Endocrinology, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing 100078, China
    c Department of Traditional Chinese Medicine, Beijing Tongren Hospital, Beijing 100730, China
    d The Third Laboratory of Pharmacology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China
  • Received:2010-01-08 Accepted:2010-04-20 Online:2010-06-20 Published:2010-06-15


To observe the effects of Tangnaikang (TNK), a compound traditional Chinese herbal medicine, on glucose metabolism and insulin resistance in obese Zucker rats.

Twelve male obese Zucker rats, 6 weeks old, were randomly divided into control group and TNK group (3.24 g/kg) after being fed for 2 weeks. All rats received high-fat diet and 4-week treatment. Body weight and blood glucose were tested every week. Oral glucose tolerance test (OGTT) was performed and fasting insulin level was tested on days 0, 14 and 28. Triglyceride, cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and free fatty acids (FFA) were tested on day 28. Glucose infusion rate (GIR) was tested by hyperinsulinemic-euglycemic clamp from day 29. The protein expressions of protein kinase B (Akt), phospho-Akt (p-Akt) (Thr308) and glucose transporter protein 4 (GLUT4) in skeletal muscle and GLUT4 in adipose tissue were measured after hyperinsulinemic-euglycemic clamp test.

Compared with the control group, the fed blood glucose level and glucose level of OGTT at 120 min had a significant decline in TNK group on day 28, and TNK caused no alteration of the fasting serum insulin, and the GIR increased significantly in hyperinsulinemic-euglycemic clamp study. Furthermore, TNK increased Akt and p-Akt (Thr308) protein expressions in skeletal muscle and decreased the protein expression of GLUT4 in white adipose tissue. Body weight, and triglyceride, cholesterol, LDL-C and FFA contents were slightly decreased in the TNK group, but there were no statistically significant effects.

TNK increases the protein expressions of Akt and p-Akt (Thr308) of the signal transduction pathway to influence the translocation of GLUT4 in skeletal muscle and improves glucose metabolism by reducing insulin resistance.

Key words: Compound (TCD), Diabetes mellitus, Type 2, Insulin resistance, Glucose transporter protein 4, Glucose clamp technique, Obese Zucker rats







Figure 1

Expressions of Akt, phospho-Akt (Thr308) and GLUT4 proteins in skeletal muscle and expression of GLUT4 protein in white adipose tissue detected by Western blotting"

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