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Chunyu Tian [1; 2] and Hong Chang [1; 2] and Xiaojin La [1; 2] and Ji-an Li [1; 2]
Academic Editor: Akhilesh K. Tamrakar
1, North China University of Science and Technology, Tangshan 063210, China, ncst.edu.cn
2, Pharmacology Analysis Key Laboratory for Prevention and Treatment of Diabetes of Traditional Chinese Medicine in Hebei Province, Tangshan 063210, China
Received Sep 8, 2017; Revised Nov 25, 2017; Accepted Dec 4, 2017
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.
1. Introduction
Diabetes mellitus characterized by deregulation of glucose and lipid metabolism seriously affects human health. It affected an estimated 366 million people in 2011 and the number is projected to be 600 million by the year 2035 [1]. Type 2 diabetes mellitus (T2DM), one of the most common types of diabetes with the characteristics of insensitivity to insulin, has attracted great attention [2]. Insulin resistance (IR), an impaired biological response to insulin, is the pathological basis of T2DM. It refers to the decreased sensitivity of tissues to insulin, resulting in the reduction in glucose uptake and utilization [3]. In the body, skeletal muscle is the main target organ that consumes glucose and completes approximately 80% of the postprandial glucose intake and consumption caused by insulin stimulation [4, 5]. However, under the condition of IR, insulin-stimulated glucose disposal in skeletal muscle is severely damaged and could not respond to insulin properly. This leads to a defect in the insulin signaling pathway in muscle and elevating blood glucose level, which is a key feature of IR in T2DM. Therefore, skeletal muscle was selected as a therapeutic target of WSZYF in the battle against T2DM.
The main proteins in the phosphatidylinositol 3-kinase (PI3K) signaling pathway, including PI3K, Akt, and glucose transporter type 4 (GLUT4), play important roles in insulin signaling transduction. The abnormality of this pathway is the major cause of T2DM [6]. The signaling cascade is triggered when insulin connects with the membrane receptor of target cells. Insulin receptor substrate-1 (IRS-1) phosphorylated by the activated insulin receptor leads to PI3K and Akt activation [7]. GLUT4, downstream of PI3K, is the pivotal protein in controlling glucose uptake...