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山东大学学报(医学版) ›› 2009, Vol. 47 ›› Issue (10): 5-8.

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脂联素对L6大鼠骨骼肌细胞葡萄糖摄取的影响

刘元涛1,倪一虹1,姜兆顺2,陈诗鸿1,庄向华1,
孙福敦1,李晓博1,潘喆1,宋慧玲1   

  1. 1. 山东大学第二医院内分泌科, 济南 250033; 2. 济南军区总医院内分泌科, 济南 250031
  • 收稿日期:2009-04-16 出版日期:2009-10-16 发布日期:2009-10-16
  • 通讯作者: 宋慧玲(1950- ),女,主任医师,主要从事内分泌基础研究与 临床工作。Email:songhuiling@medmail.com.cn
  • 作者简介:刘元涛(1965- ),男,博士(Ph.D),主要从事内分泌基础研究与临 床工作。Email:liuyuantao@yahoo.com

Effects of adiponectin on glucose uptake in L6 rat skeletal muscle cells

LIU Yuantao1, NI Yihong1, JIANG  Zhaoshun2, CHEN Shihong1, ZHUANG Xianghua1, SUN Fudun1, LI Xiaobo1, PAN Zhe1, SONG Huiling1   

  1. 1. Department of Endocrinology, Second Hospital of Shandong Univerist y, Jinan250033, China; 2. Department of Endocrinology, General Hospital of Jinan Milit ary Command, Jinan 250031, China
  • Received:2009-04-16 Online:2009-10-16 Published:2009-10-16

摘要:

目的观察脂联素对L6大鼠骨骼肌细胞基础及胰岛素诱导的葡萄糖摄取的影响。方法1. 将L6细胞分为脂联素处理组(脂联素刺激30?min)、胰岛素处理组(10?nmol/L胰岛素刺激20?mi n)和对照组。处理后分别测定各组细胞的葡萄糖摄取率。2. 将稳定表达葡萄糖转运子4(Gluosetransporter 4, GLUT4)的L6细胞(L6GLUT4细胞)分为6组:① 对照组; ② 脂联素处理组:脂联素刺激30?min;③ 低浓度胰岛素处理组:0.1?nmol/L胰岛素刺激20?min; ④ 高浓度胰岛素组:10?nmol/L胰岛素刺激20?min; ⑤ 脂联素预处理+低浓度胰岛素组:脂联素预处理30?min,0.1?nmol/L胰岛素刺激20?min; ⑥ 脂联素预处理+高浓度胰岛素组:脂联素预处理30?min,10?nmol/L胰岛素处理20?min。处理后分别测定各组细胞的葡萄糖摄取率及GLUT4细胞膜含量。结果L6细胞:脂联素处理组葡萄糖摄取率与对照组差异无统计学意义(P>0.05) 。L6GLUT4细胞:① 脂联素处理组细胞膜GLUT4含量、葡萄糖摄取率与对照组差异均无统计学意义(P均>0.05);② 低浓度胰岛素处理组细胞膜GLUT4含量、葡萄糖摄取率均显著高于对照组(P均<0.01);脂联素预处理+低浓度胰岛素组细胞膜GLUT4含量、葡萄糖摄取率均显著高于脂联素处理组(P均<0.01)以及低浓度胰岛素处理组(P均<0.01);③ 高浓度胰岛素处理组葡萄糖摄取率、细胞膜GLUT4含量均显著高于低浓度胰岛素处理组(P<0.05,P<0.01);脂联素预处理+高浓度胰岛素组与脂联素预处理+低浓度胰岛素组比较,葡萄糖摄取率显著升高(P<0.05),而GLUT4细胞膜含量升高不显著(P>0.05);脂联素预处理+高浓度胰岛素组葡萄糖摄取率显著高于单纯高浓度胰岛素组(P<0.01),而GLUT4细胞膜含量差异无统计学意义(P>0.05)。结论① 脂联素对骨骼肌细胞的葡萄糖基础摄取无明显影响;② 脂联素本身不足以诱导骨骼肌细胞的GLUT4细胞膜转位及葡萄糖摄取;③ 脂联素可增加胰岛素诱导的骨骼肌细胞的葡萄糖摄取,其机制可能与加强胰岛素诱导的GLUT4细胞膜转位以及增加细胞膜GLUT4对葡萄糖的转运效率有关。

关键词: 脂联素, 葡萄糖转运子4, 骨骼肌细胞, 葡萄糖摄取

Abstract:

To observe the effects of adiponectin on basal and insulininduced glucose uptake in L6 rat skeletal muscle myoblasts. MethodsWildtype L6 cells were divided into 3 groups: the adiponectin treatment group(stimulation with adiponectin for 30?min), the insulin treatment group(stimulation with 10?nmol/L insulin for 20?min) and the control group. After treatments, the glucose uptake of each group was determined. L6 cells stably expressing GLUT4(Glucose transporter 4)were divided into 6 groups: the control group, the adiponectin treatment group(stimulation with adiponectin for 30?min), the lower concentration of insulin group(stimulation with 0.1?nmol/L insulin for 20?min), the higher concentration of insulin group(stimulation with 10?nmol/Linsulin for 20?min), the adiponectin+lower concentration of insulin group (pretreatment with adiponectin for 30?min, then stimulation with 0.1?nmol/L insulin for 20?min), and the adiponectin+higher concentration of insulin group (pretreatment with adiponectin for 30?min, then stimulation with 10?nmol/L insulin for 20?min). After treatments, glucose uptake and plasma membrane GLUT4 content were determined.  ResultsIn wildtype L6 cells: the glucose uptake of the adiponectin treatment group was not significantly different from that of the control(P>0.05).  In L6GLUT4 cells: ① Without insulin stimulation, the glucose uptake and the plasma membrane GLUT4 content of the adiponectin treatment group were not significantly different from those of the control(P>0.05, respectively ). ② The glucose uptake and the  plasma membrane GLUT4 content of the lower concentration of insulin treatment group were both  significantly higher than those of the control (P<0.01, respectively). With lower concentration of insulin treatment, the glucose uptake and the plasma membrane GLUT4 content of cells pretreated with adiponectin were both higher than those of the adiponectin treatment group(P<0.01, respectively), and were also significantly higher than those of the lower concentration of insulin treatment group(P<0.01, respectively). ③ With higher concentration of insulin treatment, the glucose uptake and the plasma membrane GLUT4 content were further increased when compared with those with lower concentration of insulin treatment(P<0.05,  P<0.01, respectively). Compared with the adiponectin + lower concentration of insulin group, the glucose uptake of the adiponectin + higher concentration of insulin group was significantly increased(P<0.05), and was also higher than that of the higher concentration of insulin group, however the plasma membrane GLUT4 content of the adiponectin + higher concentration of insulin group was neither significantly different from that of the adiponectin + lower concentration of insulin group(P>0.05)nor that of the higher concentration of insulin treatment group(P>0.05). Conclusion① Adiponectin has no effect on basal glucose uptake of L6 rat skeletal muscle cells. ② Adiponectin alone is not sufficient to cause GLUT4 plasma membrane translocation and glucose uptake in L6 rat skeletal muscle cells. ③ Adiponectin enhances insulininduced glucose uptake in skeletal muscle cells possibly by sensitizing insulininduced GLUT4 plasma membrane translocation and by increasing the efficacy of GLUT4 mediated glucose transportation.

Key words: Adiponectin; Glucose transporter 4; Skeletal muscle c ell; Glucose uptake

中图分类号: 

  • R34
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