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Evidence-Based Complementary and Alternative Medicine
Volume 2017 (2017), Article ID 7302965, 9 pages
Research Article

Antidiabetic Effect of Tibetan Medicine Tang-Kang-Fu-San on High-Fat Diet and Streptozotocin-Induced Type 2 Diabetic Rats

1College of Basic Medicine, Hubei University of Chinese Medicine, Wuhan 430065, China
2College of Pharmaceutical Sciences, South-Central University for Nationalities, Wuhan 430074, China
3Center for the Study of Itch, Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110, USA
4Barnes-Jewish Hospital, St. Louis, MO 63110, USA
5College of Nursing & Medical Technology, Jianghan University, Wuhan 430056, China
6Department of Encephalopathy, Wuhan Hospital of Traditional Chinese Medicine, Wuhan 430014, China

Correspondence should be addressed to Tiexiang Gao and Zhinan Mei

Received 5 April 2017; Accepted 13 July 2017; Published 17 August 2017

Academic Editor: Dolores García Giménez

Copyright © 2017 Bailu Duan 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 was to investigate the antidiabetic effects of a Tibetan medicine, Tang-Kang-Fu-San (TKFS), on experimental type 2 diabetes mellitus (T2DM) rats and to explore its underlying mechanisms. Firstly two major chemical compositions of TKFS, gallic acid and curcumin, were characterized by HPLC fingerprint analysis. Next T2DM in rats was induced by high-fat diet and a low-dose streptozotocin (STZ 35 mg/kg). Then oral gavage administration of three different doses of TKFS (0.3 g/kg, 0.6 g/kg, and 1.2 g/kg) was given to T2DM rats. Experimental results showed that TKFS dramatically reduced the levels of fasting blood glucose, fasting blood insulin, triglyceride, total cholesterol, LDL cholesterol, and HDL cholesterol, even though it did not alter the animal body weight. The downregulation of phosphorylation-AKT (p-AKT) and glucose transporter-4 (GLUT4) in skeletal muscle of T2DM rats was restored and abnormal pathological changes in pancreas tissues were also improved. Our work showed that TKFS could alleviate diabetic syndromes, maintain the glucose homeostasis, and protect against insulin resistance in T2DM rats, and the improvement of AKT phosphorylation and GLUT4 translocation in skeletal muscle would be one of its possible underlying mechanisms.