Mechanism of human umbilical cord mesenchymal stem cells in improving insulin resistance in type 2 diabetic rats
10.3760/cma.j.cn115822-220200310-200061
- VernacularTitle:人脐带间充质干细胞改善2型糖尿病大鼠胰岛素抵抗的作用机制研究
- Author:
Shenghui GUO
1
;
Shiwei LIU
;
Ruixue DUAN
;
Meimei WANG
;
Yaru WU
;
Ying WEI
Author Information
1. 山西医科大学生物化学与分子生物学教研室，太原 030001
- From:
Chinese Journal of Clinical Nutrition
2020;28(2):93-100
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To observe the therapeutic effects of human umbilical cord mesenchymal stem cells (HUC-MSCs) on insulin resistance, and to investigate the molecular mechanisms in T2DM rats.Methods:The T2DM rats were induced by a high fat and high glucose diet for 10 weeks combined with low-dose streptozocin. Four weeks after infusion of HUC-MSCs via tail vein of the rats, fasting blood glucose, triglycerides, cholesterol were measured. Intraperitoneal glucose tolerance test, intraperitoneal insulin tolerance test and hyperinsulinemic-euglycaemic clamp test were performed to evaluate the islet function and insulin resistance level of rats. The protein expression levels of lipid metabolism signal pathway adenine monophosphate activated protein kinase (AMPK) and acetyl CoA carboxylase (ACC) in liver tissue were detected by western blot.Results:Compared with the T2DM group, HUC-MSCs treatment can significantly reduce fasting blood glucose, triglycerides, total cholesterol levels ( P<0.01), and the values of area under the curve of glucose tolerance and insulin tolerance ( P<0.05) in the T2DM+ HUC-MSCs group. Hyperinsulinemic-euglycaemic clamp test found that compared with the T2DM group, after HUC-MSCs treatment, the glucose infusion rate level was significantly higher in the T2DM+ HUC-MSCs group( P<0.01); Western blot showed that compared with the T2DM group, the ratio of p-AMPK to AMPK and p-ACC to ACC in liver tissues of T2DM+ HUC-MSCs group were significantly increased( P<0.01). Conclusion:Human umbilical cord mesenchymal stem cells treatment may improve lipid metabolism and insulin resistance by activating AMPK/ACC signaling pathways in type 2 diabetic rats.
