脂肪细胞缺氧对骨骼肌细胞胰岛素作用的影响

目的：观察脂肪细胞缺氧对骨骼肌细胞胰岛素作用的影响。方法：缺氧（5％CO2、85％N2、10％H2或200μmol／L CoCl2）处理小鼠3T3-L1脂肪细胞，制备条件培养基孵育小鼠骨骼肌细胞。通过对胰岛素信号通路中关键蛋白的磷酸化水平和葡萄糖转运子4（GLUT4）转位得以检测骨骼肌胰岛素作用的改变。结果：缺氧处理的3T3-L1脂肪细胞条件培养基抑制骨骼肌胰岛素信号通路，其中胰岛素受体底物10RS1Set307）磷酸化水平呈显著增高，相反蛋白激酶B（AktSer473）磷酸化水平呈显著下降，最终显著抑制了胰岛素刺激的GLUT4myc转位（p〈0．05）。结论：抑制胰岛素刺激的GLUT4myc转位，其机制与IRSt的Ser307的磷酸化水平升高和Akt的Ser473的磷酸化水平降低有关。

The effect of hypoxia of adipocytes on insulin function in skeletal muscle cells

Objective： To investigate the effect of hypoxia of adipocytes on the insulin function in skeletal muscle cells. Methods： 3T3-L1 adipocytes were treated with hypoxia by incubating at 5% CO2, 85% N2, 10% HE or with 200 μmolL CoCl2. The conditioned medium from 3T3-LI adipocytes was used to incubate skeletal muscle cells. The change of the insulin function was studied by detection of phosphorylation of insulin signal molecules and the translocation of glucose transport 4 （GLUT4）. Results： The conditioned medium from hypoxia-treated 3T3-L1 adipocytes inhibited insulin signaling pathway by increased the phosphorylation of insulin receptor substrate 1 （IRS1 Ser307）, decreased the phosphorylation of protein kinase B （Akt Ser473）, therefore inhibited GLUT4rnyc translocation in response to insulin （P〈0.05）. Conclusion： The conditioned medium from hypoxia-treated adipocytes inhibits insulin function.The mechanism may relate to the increase of phosphorylation of IRSI Set307 and decrease of the phosphorylation Akt 5er473.