【摘要】 目的　探讨过氧钒烟酸络合物（ＰＯＲ）对胰岛素抵抗的逆转作用，ＰＯＲ促进葡萄糖摄取与胰岛素促进作用在机制上的异同。方法方法　以皮下渗透式输注ＰＯＲ，观察ＰＯＲ对Ｚｕｃｋｅｒ大鼠胰岛素抵抗的缓解作用，检测ＰＯＲ对具有胰岛素严重抵抗的Ｚｕｃｋｅｒ肥胖大鼠睾丸脂肪垫脂肪细胞对葡萄糖摄取的促进作用，以及对ＰＬ－３Ｋ Ｐ１１０亚单位酪氨酸磷酸化的影响，比较ＰＯＲ和胰岛素促进ＧＬＵＴ４的转位对ＰＩ－３Ｋ的依赖性。结果　ＰＯＲ可以使肥胖伴胰岛素抵抗大鼠的空腹血糖明显降低，对糖负荷的处理能力明显提高；ＧＴＴ曲线下胰岛素的水平明显降低，提示对胰岛素的敏感性提高。葡萄糖载体的转位水平与ＰＩ－３Ｋ活性并不平行，胰岛素促进的葡萄糖摄取作用对ＰＩ－３Ｋ有依赖性，过氧钒络合物（ＰＯＲ）对葡萄糖载体转位的促进作用不依赖于ＰＩ－３Ｋ，表现为ＰＯＲ促进的葡萄糖摄取下被ＰＩ－３Ｋ抑制剂（Ｗｏｒｔｍａｎｎｉｎ）抑制。结论　ＰＯＲ在１／１０钒酸盐剂量下能逆转Ｚｕｃｋｅｒ大鼠的胰岛素抵抗，胰岛素对葡萄糖载体的激活作用是ＰＩ－３Ｋ依赖性的，而过氧钒（ＰＯＲ）则可通过其他途径激活葡萄糖载体，具体机制可能与载体的直接激活有关。更多还原

【Abstract】 Objective To investigate the Peroxovanadate reversing insulin resistance in Zucker obese rats and demonstrate the relationship of activation of PI-3 kinase and glucose uptake or Glut4 translocation upon insulin stimulation and POR pretreatment. Methods Glucose uptake and Glut4 translocation in epididymal adipocytes were measured by using 2-DG and fat cell homogenates undergone different speed of centrifugation to generate plasma membrance (PM) and low density membrance (LDM). Results POR and insulin both activated PI-3 Kinase and glucose uptake. PI-3 kinase inhibitor (wortmannin) can block insulin stimulated glucose uptake and Glut4 translocation, but wortmannin can not inhibit POR induced glucose uptake and translocation. Conclusion Our results suggested that Peroxovanadate nicotinic complexes (POR) reversed insulin resistance in Zucker obese rats. POR induced activation of Glucose transporter (Glut4) in vitro is PI-3 Kinase independent compare to insulin stimulated glucose uptake and Glut4 translocation is wortmannin sensitive.更多还原