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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30min)、胰岛素处理组(10nmol/L胰岛素刺激20min)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(Gluosetransporter4,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30min;③低浓度胰岛素处理组:0.1nmol/L胰岛素刺激20min;④高浓度胰岛素组:10nmol/L胰岛素刺激20min;⑤脂联素预处理+低浓度胰岛素组:脂联素预处理30min,0.1nmol/L胰岛素刺激20min;⑥脂联素预处理+高浓度胰岛素组:脂联素预处理30min,10nmol/L胰岛素处理20min。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。
Objective To observe the effects of adiponectin on the basis of skeletal muscle cells and insulin-induced glucose uptake in L6 rats. L6 cells were divided into adiponectin group (adiponectin stimulation 30min), insulin treatment group (10nmol / L insulin stimulation 20min) and control group. After treatment, the glucose uptake rate of each group of cells was determined. The L6 cells (L6-GLUT4 cells) stably expressing glucose transporter 4 (GLUT4) were divided into 6 groups: ① control group; ② adiponectin group: adiponectin stimulation for 30 min; ③ low concentration of insulin treatment Group: 0.1nmol / L insulin stimulation for 20min; ④high concentration insulin group: 10nmol / L insulin stimulation for 20min; ⑤adiponectin preconditioning + low concentration insulin group: pretreatment with adiponectin for 30min and 0.1nmol / L insulin for 20min; ⑥ adiponectin pretreatment + high concentration of insulin group: adiponectin pretreatment 30min, 10nmol / L insulin treatment 20min. After treatment, the glucose uptake rate and GLUT4 cell membrane content in each group were determined. Results There was no significant difference in glucose uptake between L6 cells and adiponectin groups and the control group (P> 0.05). L6-GLUT4 cells: ① There was no significant difference in GLUT4 content and glucose uptake in cell membrane between adiponectin group and control group (all P> 0.05); ② GLUT4 content and glucose uptake rate in low concentration insulin group were significantly higher (P <0.01). The GLUT4 content and glucose uptake rate in adiponectin + low concentration insulin group were significantly higher than those in adiponectin group (P <0.01) and low concentration insulin group (P <0.05, P <0.01). The glucose uptake rate and cell membrane GLUT4 content in high concentration insulin treatment group were significantly higher than those in low concentration insulin treatment group (P <0.05, P <0.01) Glucose uptake rate was significantly increased (P <0.05), while the GLUT4 cell membrane content was not significantly increased (P> 0.05) compared with the preconditioning + low concentration insulin group. Glucose uptake rate was significantly higher in adiponectin + high concentration insulin group (P <0.01), while there was no significant difference in the content of GLUT4 cell membrane between the two groups (P> 0.05). Conclusion ① Adiponectin has no obvious effect on glucose uptake in skeletal muscle cells; ② Adiponectin itself is not enough to induce GLUT4 cell membrane translocation and glucose uptake in skeletal muscle cells; ③ Adiponectin can increase insulin-induced skeletal muscle cells The mechanism of glucose uptake may be related to enhancing the insulin-induced translocation of GLUT4 and increasing the glucose transport efficiency of GLUT4.