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AdipoRon对小鼠骨骼肌细胞胰岛素敏感性的影响及其机制
引用本文:肖敏,屈小虎,陈慧,金丽琴. AdipoRon对小鼠骨骼肌细胞胰岛素敏感性的影响及其机制[J]. 中国应用生理学杂志, 2017, 33(4): 319-322. DOI: 10.12047/j.cjap.5533.2017.078
作者姓名:肖敏  屈小虎  陈慧  金丽琴
作者单位:温州医科大学检验医学院、生命科学学院, 浙江 温州 325035
基金项目:2015年度浙江省公益技术应用研究计划(实验动物,2015C37099)
摘    要:目的:观察脂联素受体激动剂AdipoRon对小鼠成肌细胞株(C2C12)胰岛素敏感性的影响,并探讨其作用机制。方法:使用马血清将C2C12诱导分化为成肌细胞,分为6组(9个复孔):空白对照组、AdipoRon (脂联素受体激动剂)高剂量组、AdipoRon低剂量组、胰岛素组以及AdipoRon低剂量+PI3K (磷脂酰肌醇3激酶)抑制剂组和胰岛素+PI3K抑制剂组,作用12 h,收集上清检测葡萄糖消耗量,使用CCK8测定细胞增殖。六孔板中将C2C12诱导分化为肌管细胞,加入药物作用12 h,并用RT-PCR法检测GLUT4的mRNA水平。结果:与空白对照组相比,AdipoRon高剂量组、AdipoRon低剂量组、胰岛素组耗糖量均有所增加,具有统计学意义(P<0.05)。加入PI3K抑制剂组后,耗糖量与空白对照组无统计学意义。与空白对照组相比,AdipoRon高剂量组、AdipoRon低剂量组、胰岛素组细胞均有增殖,但只有胰岛素组具有统计学意义(P<0.05)。与对照空白组相比,AdipoRon高剂量组、AdipoRon低剂量组、胰岛素组GLUT4mRNA水平均有所提高,具有统计学意义(P<0.05)。加入PI3K抑制剂组后,GLUT4mRNA水平与空白对照组无统计学意义。结论:AdipoRon能够不影响细胞增殖的情况下增加葡萄糖的消耗量,这可能是通过提高胰岛素敏感性发挥作用的,但具体机制尚待进一步的研究。

关 键 词:胰岛素敏感性  脂联素受体激动剂  PI3K  小鼠成肌细胞株(C2C12)  
收稿时间:2016-11-28

The effect of AdipoRon on insulin sensitivity of mouse skeletal muscle cells and its mechanism
XIAO Min,QU Xiao-hu,CHEN Hui,JIN Li-qin. The effect of AdipoRon on insulin sensitivity of mouse skeletal muscle cells and its mechanism[J]. Chinese journal of applied physiology, 2017, 33(4): 319-322. DOI: 10.12047/j.cjap.5533.2017.078
Authors:XIAO Min  QU Xiao-hu  CHEN Hui  JIN Li-qin
Affiliation:Department of Biology, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou 325035, China
Abstract:Objective: To observe the effect of AdipoRon, an adiponin receptor agonist, on insulin sensitivity in mouse myoblast cell line (C2C12) and to explore its mechanism.Methods: C2C12 was induced to differentiate into myoblasts by using horse serum. Then the cells were divided into 6 groups (9 double wells):blank control group, high dose AdipoRon group, low dose AdipoRon group, insulin group and the low dose AdipoRon with PI3K inhibitor (phosphatidylinositol 3 kinase) group and the insulin with PI3K inhibitor group. After cultured for 12 h, the supernatant was collected and glucose consumption was measured. Cell proliferation was tested by using CCK8. In the 6-well plate, C2C12 was induced to differentiate into myoblasts. The drug was incubated for 12 h and the mRNA level of GLUT4 was detected by RT-PCR.Results: Compared with the blank control group, the levels of glucose consumption in high dose AdipoRon group, low dose AdipoRon group and insulin group was increased significantly (P<0.05). After adding PI3K inhibitor, the levels of glucose consumption in the above mentioned three groups were not different from that in blank control group. high dose AdipoRon group, low dose AdipoRon group and insulin group had proliferation, but only the insulin group was statistically significant (P<0.05). Compared with the control group, the levels of GLUT4 mRNA in AdipoRon high dose group, low dose AdipoRon group and insulin group were all higher than those in control group (P<0.05). After adding PI3K inhibitor, GLUT4 mRNA level was not statistically significant compared with blank control group.Conclusion: AdipoRon can increase the consumption of glucose without affecting cell proliferation, which may play a role in improving insulin sensitivity, but the specific mechanism remains to be further studied.
Keywords:insulin resistance  AdipoRon  PI3K  mouse myoblast cell line (C2C12)  
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