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利拉鲁肽对小鼠骨骼肌细胞葡萄糖转运子4转位的作用
  • ISSN号:1674-5809
  • 期刊名称:《中华糖尿病杂志》
  • 时间:0
  • 分类:R587.1[医药卫生—内分泌;医药卫生—临床医学;医药卫生—内科学]
  • 作者机构:[1]天津医科大学代谢病医院,卫生部激素与发育重点实验室,天津300070, [2]天津医科大学免疫学系
  • 相关基金:国家自然科学基金面上项目(81170740);国家自然科学基金国际合作项目(81161120545);高等学校博士学科点专项基金(20121202110014)
中文摘要:

目的 探讨胰高血糖素样肽1 (GLP-1)类似物利拉鲁肽对小鼠骨骼肌细胞葡萄糖转运子4(GLUT4)转位的作用及可能机制.方法 在过表达带有HA表位GLUT4的小鼠骨骼肌细胞株C2C12(C2C12-GLUT4H),分为正常对照组、胰岛素组(100 nmol/L)、利拉鲁肽1组(100 nmol/L)、利拉鲁肽2组(1 000 nmol/L)、5-氨基咪唑-4-甲酰1-β-D呋喃糖苷(AICAR)(腺苷酸活化蛋白激酶激动剂)组(2 mmol/L).通过ELISA法测定细胞膜上C2C12-GLUT4HA,检测各组对C2C12-GLUT4HA细胞GLUT4转位的作用.应用Western blotting检测介导GLUT4转位的信号分子蛋白激酶B(AKT)、腺苷酸活化蛋白激酶(AMPK)磷酸化水平以及GLUT4蛋白表达水平.采用Student's t检验或单因素方差分析进行统计分析.结果 利拉鲁肽组的GLUT4转位较对照组相比明显上升[分别是对照组的(1.53±0.28)倍、(1.41±0.41)倍,F=13.4798,P<0.05];利拉鲁肽刺激组与对照组相比能够使pAMPK水平升高[分别是对照组的(1.79±0.31)倍、(1.54±0.18)倍,F=20.0999,P<0.05],而对pAKT无明显影响(P>0.05).结论 利拉鲁肽可通过激活AMPK从而促进小鼠骨骼肌细胞GLUT4转位的增加.

英文摘要:

Objective To investigate the effects and mechanism of glucagon-likepeptide1(GLP-1) analogue liraglutide on glucose transporter 4 (GLUT4) translocation of mouse skeletal muscle cells.Methods In overexpressing C2C12-GLUT4HA cells,observing the effects and molecular mechanism of liraglutide on GLUT4 translocation.C2C12-GLUT4HA cells were divided into the control group,insulin group(100 nmol/L),liraglutide Ⅰ group(100 nmo]/L),liraglutide Ⅱ group(1 000 nmol/L),5-aminoimidazole-4-carboxamide 1-β-D-ribofuranoside (AICAR) (adenosine 5'-monophosphate (AMP)-activated protein kinase agonist) group (2 mmol/L).The amount of GLUT4HA on the cell surface was measured by enzyme-linked immunosorbent assay(ELISA).The phosphorylation of adenosine 5'-monophosphate (AMP)-activated protein kinase(AMPK),protein kinases B (AKT),and GLUT4 expression were tested by western blotting.Statistical analyses were performed using Student's t test or analysis of variance (ANOVA).Results The amount of GLUT4HA on the cell surface in liraglutide groups was more than the amount of GLUT4HA on the cell surface in control group (1.53±0.28 vs 1.41±0.41,F=13.4798,P〈0.05).The expression of GLUT4 was not changed in liraglutide groups and the control group.The levels of phosphorylation of AMPK were more in liraglutide groups than that in the control group(1.79±0.31 vs 1.54±0.18,respectively,F=20.0999,P〈0.05).But the phosphorylation of AKT was not changed(P〉0.05).Conclusion This study suggests that Liraglutide may induce GLUT4 translocation of mouse skeletal cells by activation of AMPK.

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期刊信息
  • 《中华糖尿病杂志》
  • 中国科技核心期刊
  • 主管单位:中国科学技术协会
  • 主办单位:中华医学会
  • 主编:
  • 地址:北京市东四西大街42号
  • 邮编:100710
  • 邮箱:office@cma.org.cn
  • 电话:010-85158180
  • 国际标准刊号:ISSN:1674-5809
  • 国内统一刊号:ISSN:11-5791/R
  • 邮发代号:80-994
  • 获奖情况:
  • 国内外数据库收录:
  • 被引量:4248