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配方通过蛋白酪氨酸磷酸酶1B-胰岛素受体底物1-蛋白激酶B-葡萄糖转运蛋白4信号通路改善2型糖尿病患者骨骼肌胰岛素抵抗。

Formula Improves Skeletal Muscle Insulin Resistance in Type 2 Diabetes Mellitus via PTP1B-IRS1-Akt-GLUT4 Signaling Pathway.

作者信息

Tian Chunyu, Chang Hong, La Xiaojin, Li Ji-An

机构信息

North China University of Science and Technology, Tangshan 063210, China.

Pharmacology Analysis Key Laboratory for Prevention and Treatment of Diabetes of Traditional Chinese Medicine in Hebei Province, Tangshan 063210, China.

出版信息

Evid Based Complement Alternat Med. 2017;2017:4393529. doi: 10.1155/2017/4393529. Epub 2017 Dec 31.

Abstract

formula (WSZYF) is an effective traditional Chinese medicine in the treatment of type 2 diabetes mellitus (T2DM). This study aimed to identify the effects and underlying mechanisms of WSZYF on improving skeletal muscle insulin resistance in T2DM. 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. , WSZYF improved general conditions and decreased significantly fasting blood glucose, glycosylated serum protein, glycosylated hemoglobin, insulin concentration, and insulin resistance index of T2DM rats. , 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. . 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.

摘要

五参芪药方剂(WSZYF)是治疗2型糖尿病(T2DM)的一种有效中药。本研究旨在确定WSZYF改善T2DM患者骨骼肌胰岛素抵抗的作用及潜在机制。通过给Goto-Kakizaki糖尿病倾向大鼠喂食高脂高糖饲料4周诱导建立T2DM动物模型。在骨骼肌细胞中诱导建立胰岛素抵抗模型。结果显示,WSZYF改善了T2DM大鼠的一般状况,并显著降低了空腹血糖、糖化血清蛋白、糖化血红蛋白、胰岛素浓度和胰岛素抵抗指数。此外,WSZYF增强了骨骼肌细胞胰岛素抵抗模型中的葡萄糖消耗。此外,WSZYF影响了调节T2DM的分子表达,包括增加p-IRS1、p-Akt和GLUT4的表达,降低PTP1B表达。这些发现显示了WSZYF作为治疗T2DM的新药候选物的潜力,且WSZYF的抗糖尿病机制可能是通过调节PTP1B-IRS1-Akt-GLUT4信号通路介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fb5/5804399/eb0741f8b118/ECAM2017-4393529.001.jpg

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