Jiaotai pill (a0currency signae3°a) enhances insulin signaling through phosphatidylinositol 3-kinase pathway in skeletal muscle of diabetic rats

被引:11
作者
Dong Hui [1 ]
Wang Jian-hong [1 ]
Lu Fu-er [1 ]
Xu Li-jun [1 ]
Gong Yan-lin [1 ]
Zou Xin [1 ]
机构
[1] Huazhong Univ Sci & Technol, Inst Integrat Tradit Chinese & Western Med, Tongji Hosp, Tongji Med Coll, Wuhan 430030, Peoples R China
基金
中国国家自然科学基金;
关键词
Jiaotai Pill; insulin signaling; phosphatidylinositol; 3-kinase; skeletal muscle; diabetes mellitus; Chinese medicine; THIAZOLIDINEDIONE USE; COPTIDIS-RHIZOMA; TYPE-2; MELLITUS; CINNAMON; BERBERINE; GLUCOSE; PREVALENCE; RESISTANCE; CHINA;
D O I
10.1007/s11655-013-1560-1
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
To investigate the effect of Jiaotai Pill (a(0)currency signae(3)degrees a, JTP) at different constitutional proportions on insulin signaling through phosphatidylinositol 3-kinase (PI3K) pathway in the skeletal muscle of diabetic rats. 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. All the three formulations of JTP decreased plasma glucose and fasting insulin levels as well as increased the protein expressions of insulin receptor beta (InsR beta) 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 InsR beta 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. 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.
引用
收藏
页码:668 / 674
页数:7
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