Hypoglycemic effect of D-chiro-inositol in type 2 diabetes mellitus rats through the PI3K/Akt signaling pathway

被引：64
作者：
Gao, Yun-feng [1 ]
Zhang, Meng-na [1 ]
Wang, Tian-xin [1 ]
Wu, Tian-chen [1 ]
Ai, Ru-dan [1 ]
Zhang, Ze-sheng [1 ]
机构：
[1] Tianjin Univ Sci & Technol, Coll Food Engn & Biotechnol, Minist Educ, Key Lab Food Nutr & Safety, Tianjin 300457, Peoples R China
来源：
MOLECULAR AND CELLULAR ENDOCRINOLOGY | 2016年 / 433卷 / 0C期
关键词：
D-chiro-inositol; Diabetes mellitus; PI3K/Akt signaling pathway; Liver tissue; Skeletal muscle; HIGH-FAT DIET; BETA-CELL DYSFUNCTION; HUMAN SKELETAL-MUSCLE; INSULIN-RESISTANCE; PPAR-GAMMA; PATHOPHYSIOLOGY; HYPERGLYCEMIA; PREVENTION; GLUT4;
D O I：
10.1016/j.mce.2016.05.013
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
In this investigation, a model of type 2 diabetes mellitus (T2DM) was used on Sprague-Dawley (SD) rats to clarify more details of the mechanism in the therapy of T2DM. D-chiro-inositol (DCI) was administrated to the diabetic rats as two doses [30, 60 mg/(kg.body weight.day)]. The biochemical indices revealed that DCI had a positive effect on hypoglycemic activity and promoted the glycogen synthesis. The rats in DCI high-dosage group had a blood glucose reduction rate of 21.5% after 5 weeks of treatment, and had insulin content in serum about 15.3 +/- 2.37 mIU/L which was significantly decreased than diabetes control group. Real-time polymerase chain reaction (RT-PCR) results revealed that DCI gave a positive regulation on glycogen synthase (GS) and protein glucose transporter-4 (Glut4). Western blotting suggested that DCI could up-regulated the expression of the phosphatidylinositol-3-kinase (PI3K) p85, PI3Kp110, GS as well as the phosphorylation of protein kinase B (Akt) both in the liver and the skeletal muscle. The results also revealed that DCI enhanced the Glut4 expression on skeletal muscle. Above all, DCI played a positive role in regulating insulin-mediated glucose uptake through the PI3K/Akt signaling pathway in T2DM rats. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码：26 / 34
页数：9
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