调查 Jiaotai 药片的效果的目的(, JTP ) 在胰岛素通过 phosphatidylinositol 3-kinase (PI3K ) 发信号上的不同宪政的比例在糖尿病的老鼠的骨胳的肌肉的小径。类型 2 糖尿病 mellitus (T2DM ) 的老鼠模型被 streptozotoein 的小剂量的静脉内的注射加高脂肪建立的方法节食喂。在黄棕色的一样的剂量和黄连属 chinensis 的增加的剂量的 JTP 分别地予糖尿病的老鼠被以九个星期。血浆葡萄糖和胰岛素层次是 assayed。蛋白质的表情被西方的污点方法决定。结果 JTP 的所有三明确的表达减少了血浆葡萄糖和 fasting 胰岛素层次象一样增加了胰岛素受体(InsR ) 的蛋白质表情子单元,胰岛素受体 substrate-1 (IRS-1 ) , PI3K p85 子单元和葡萄糖 transporter 4 (GLUT4 ) 在里面骨胳的肌肉。同时, JTP 增加了 InsR 子单元和 IRS-1 的酷氨酸 phosphorylation,并且在骨胳的肌肉减少了 IRS-1 的丝氨酸 phosphorylation。有趣地,改进胰岛素敏感上的 JTP 的效果不是剂量依赖者。相反,包含黄连属 chinensis 的最少的数量的 JTP 展出了最好的效果。在不同宪政的比例的结论 JTP 在 T2DM 的一个老鼠模型稀释糖尿病的发展。机制可能与提高胰岛素在骨胳的肌肉通过 PI3K 小径发信号被联系。
objective: To investigate the effect of Jiaotai Pill (交泰丸, JTP) at different constitutional proportions on insulin signaling through phosphatidylinositol 3-kinase (PI3K) pathway in the skeletal muscle of diabetic rats. Methods: The rat model of type 2 diabetes mellitus (T2DM) was established by intravenous injection of a small dose of streptozotoein plus high fat diet feeding. JTP at the same dosage of cinnamon and the increasing dosage of Coptis chinensis was administered to diabetic rats for nine weeks respectively. Plasma glucose and insulin levels were assayed. The expressions of proteins were determined by Western blot method. Results: All the three formulations of JTP decreased plasma glucose and fasting insulin levels as well as increased the protein expressions of insulin receptor β (InsR β) subunit, insulin receptor substrate-1 (IRS-1), PI3K p85 subunit and glucose transporter 4 (GLUT4) in skeletal muscle. Meanwhile, JTP increased the tyrosine phosphorylation of InsRβ subunit and IRS-1, and reduced the serine phosphorylation of IRS-1 in skeletal muscle. Interestingly, the effect of JTP on improving insulin sensitivity was not dose-dependent. In contrast, JTP containing the least amount of Coptis chinensis exhibited the best effect. Conclusion: JTP at different constitutional proportions attenuates the development of diabetes in a rat model of T2DM. The mechanism might be associated with enhancing insulin signaling through PI3K pathway in the skeletal muscle.