摘要
用地塞米松和胰岛素长期作用3T3 L1脂肪细胞产生胰岛素抵抗,用胰岛素增敏剂罗格列酮改善胰岛素抵抗,微量化GOD POD法检测培养基中残存的葡萄糖,并检测细胞中葡萄糖转运子Glut4基因和蛋白及胰岛素信号传递元件IRS 1的基因变化.探讨了地塞米松和胰岛素诱导3T3 L1脂肪细胞产生胰岛素抵抗的机理.结果发现:①地塞米松和胰岛素诱导3T3 L1脂肪细胞产生胰岛素抵抗,细胞对葡萄糖的摄取减少.罗格列酮改善抵抗后,葡萄糖的摄取较抵抗组增加.②抵抗时,葡萄糖转运子Glut4基因和蛋白水平明显降低,改善后基因表达上调显著,蛋白水平升高,介于正常对照组与抵抗组之间.③IRS 1在抵抗时下调,用罗格列酮改善后,IRS 1的基因水平无明显变化.
Insulin resistance is formed after chronic treatment of dexamethasone and insulin. Then it is improved by rosiglitasone, an insulin enhancer. And again, glucose remained in medium was detected in a minimal way of GODPOD method. The mRNA, protein of glucose transporter Glut4 and IRS1 gene are also tested. It is shown that: ① Dexamethasone and insulin induced the insulin resistance in 3T3L1 adipocyte, glucose uptake by cells deceased. after improvement of rosiglitasone, the glucose uptake increased, but still lower than that in normal cells. ② Glut4 mRNA and protein were declined when cells were simultaneously treated with both dexamethasone and insulin,but after improvement by rosiglitasone,both mRNA and protein increased, between those of normal control and insulin resistance cells. ③ mRNA of IRS1 deceased during insulin resistance, and keep this level even after treatment of rosiglitasone.
出处
《西南师范大学学报（自然科学版）》
CAS
CSCD
北大核心
2003年第3期460-464,共5页
Journal of Southwest China Normal University(Natural Science Edition)
