Yanbo Fan1, Zhiwei He2, Wei Wang3, Jingjing Li4, Aimin Hu5, Li Li3, Ling Yan5, Zhijie Li6, Qiang Yin7. 1. Science and Education Department, Wuhan Hospital of Traditional Chinese Medicine, Wuhan, Hubei 430014, PR China; Post-doctoral Research Center of Mayinglong Pharmaceutical Group Co., Ltd., Wuhan, Hubei 430060, PR China. 2. Department of pharmacy, Xiangyang Hospital of Traditional Chinese Medicine, Xiangyang, Hubei 441099, PR China. 3. Department of Pharmacy, Wuhan Hospital of Traditional Chinese Medicine, Wuhan, Hubei 430014, PR China. 4. College of Basic Medicine, Hubei University of Chinese Medicine, Wuhan, Hubei 430065, PR China. 5. Endocrinology Department, Wuhan Hospital of Traditional Chinese Medicine, Wuhan, Hubei 430014, PR China. 6. Department of Encephalopathy, Wuhan Hospital of Traditional Chinese Medicine, Wuhan, Hubei 430014, PR China. 7. Department of Management, Xinjiang Uygur Pharmaceutical Co., Ltd., Wulumuqi, Xinjiang 830001, PR China. Electronic address: qiangy_0405@163.com.
Abstract
AIM: Previous clinical studies have demonstrated that tangganjian (TGJ), a modern Chinese prescribed medicine, has a clinical effect in the treatment of type 2 diabetes mellitus (T2DM) with nonalcoholic fatty liver disease (NAFLD). Our study aimed to investigate whether the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway is involved in this therapeutic effect. MATERIALS AND METHODS: T2DM and NAFLD rat models were constructed and treated with three different concentrations of TGJ. Pioglitazone was used as a positive control, along with the model and normal groups. For analyses, blood and livers were collected. Levels of glucose and lipid metabolism indicators, including fasting insulin and total cholesterol, were determined. The expression levels of insulin receptor substrate (IRS), PI3K, and AKT were also determined by western blotting and immunohistochemistry. Liver tissues were stained with hematoxylin & eosin. RESULTS: In the high-dose TGJ-treated and positive groups, there was a significant increase in the HDL-C level and decreases in the levels of the fasting blood glucose, 2 h postprandial blood glucose, fasting insulin, triglyceride, total cholesterol, and low-density lipoprotein cholesterol, along with a significant increase in the expression of IRS, PI3K, and AKT in the liver. TGJ could also attenuate or counteract the effects of T2DM and NAFLD in the liver lobules. CONCLUSION: A high concentration of TGJ can improve glucose and lipid metabolism by activating the IRS/PI3K/AKT signaling pathway.
AIM: Previous clinical studies have demonstrated that tangganjian (TGJ), a modern Chinese prescribed medicine, has a clinical effect in the treatment of type 2 diabetes mellitus (T2DM) with nonalcoholic fatty liver disease (NAFLD). Our study aimed to investigate whether the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway is involved in this therapeutic effect. MATERIALS AND METHODS: T2DM and NAFLD rat models were constructed and treated with three different concentrations of TGJ. Pioglitazone was used as a positive control, along with the model and normal groups. For analyses, blood and livers were collected. Levels of glucose and lipid metabolism indicators, including fasting insulin and total cholesterol, were determined. The expression levels of insulin receptor substrate (IRS), PI3K, and AKT were also determined by western blotting and immunohistochemistry. Liver tissues were stained with hematoxylin & eosin. RESULTS: In the high-dose TGJ-treated and positive groups, there was a significant increase in the HDL-C level and decreases in the levels of the fasting blood glucose, 2 h postprandial blood glucose, fasting insulin, triglyceride, total cholesterol, and low-density lipoprotein cholesterol, along with a significant increase in the expression of IRS, PI3K, and AKT in the liver. TGJ could also attenuate or counteract the effects of T2DM and NAFLD in the liver lobules. CONCLUSION: A high concentration of TGJ can improve glucose and lipid metabolism by activating the IRS/PI3K/AKT signaling pathway.