Abstract

Background. Wushenziye formula (WSZYF) is an effective traditional Chinese medicine in the treatment of type 2 diabetes mellitus (T2DM). Aim. This study aimed to identify the effects and underlying mechanisms of WSZYF on improving skeletal muscle insulin resistance in T2DM. Methods. An animal model of T2DM was induced by Goto-Kakizaki diabetes prone rats fed with high fat and sugar for 4 weeks. Insulin resistance model was induced in skeletal muscle cell. Results. In vivo, WSZYF improved general conditions and decreased significantly fasting blood glucose, glycosylated serum protein, glycosylated hemoglobin, insulin concentration, and insulin resistance index of T2DM rats. In vitro, WSZYF enhanced glucose consumption in insulin resistance model of skeletal muscle cell. Furthermore, WSZYF affected the expressions of molecules in regulating T2DM, including increasing the expressions of p-IRS1, p-Akt, and GLUT4, reducing PTP1B expression. Conclusion. These findings displayed the potential of WSZYF as a new drug candidate in the treatment of T2DM and the antidiabetic mechanism of WSZYF is probably mediated through modulating the PTP1B-IRS1-Akt-GLUT4 signaling pathway.

Highlights

  • Diabetes mellitus characterized by deregulation of glucose and lipid metabolism seriously affects human health

  • The primary antibodies against Protein tyrosine phosphatase-1B (PTP1B), p-Akt, glucose transporter type 4 (GLUT4), and GAPDH were from Bioworld Technology (USA) and antibody against p-IRS1 was from Abcam (USA)

  • These results indicated that Wushenziye formula (WSZYF) could ameliorate the general conditions of type 2 diabetes mellitus (T2DM) rats

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Summary

Introduction

Diabetes mellitus characterized by deregulation of glucose and lipid metabolism seriously affects human health. 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]. 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. Aim. This study aimed to identify the effects and underlying mechanisms of WSZYF on improving skeletal muscle insulin resistance in T2DM. WSZYF enhanced glucose consumption in insulin resistance model of skeletal muscle cell. These findings displayed the potential of WSZYF as a new drug candidate in the treatment of T2DM and the antidiabetic mechanism of WSZYF is probably mediated through modulating the PTP1B-IRS1-Akt-GLUT4 signaling pathway

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