高浓度胰岛素、葡萄糖对HepG2细胞蛋白激酶C活性的影响  

Effects of high concentrations of insulin and glucose on the protein kinase C activities of HepG2 cells

作　　者：叶娟 李果 陈家伦 

机构地区：[1]上海市第二医科大学附属瑞金医院,上海市内分泌研究所200025

出　　处：《中华内分泌代谢杂志》1999年第5期294-297,共4页Chinese Journal of Endocrinology and Metabolism

基　　金：教育部留学回国人员科研启动基金

摘　　要：目的　研究高浓度胰岛素、葡萄糖对ＨｅｐＧ２ 细胞蛋白激酶Ｃ（ＰＫＣ） 活性的影响。方法建立具胰岛素抵抗特性受体下调的ＨｅｐＧ２（ＤＲＨｅｐＧ２）细胞模型，测定１０－ ７ ｍｏｌ／Ｌ胰岛素、２５ ｍ ｍｏｌ／Ｌ葡萄糖对未处理ＨｅｐＧ２（ＮＤＲＨｅｐＧ２）细胞和ＤＲＨｅｐＧ２ 细胞膜ＰＫＣ、胞浆ＰＫＣ活性的影响。结果ＤＲＨｅｐＧ２ 细胞未受高浓度胰岛素、葡萄糖刺激时膜和胞浆ＰＫＣ活性均高于ＮＤＲＨｅｐＧ２ 细胞（ Ｐ＜０．０５）。１０ －７ ｍｏｌ／Ｌ胰岛素刺激ＮＤＲＨｅｐＧ２ 细胞或ＤＲＨｅｐＧ２ 细胞，３０ 秒和５ ～１０ 分时膜ＰＫＣ活性增高，胞浆ＰＫＣ 活性降低（ Ｐ＜ ０．０１）。２５ ｍｍｏｌ／Ｌ 葡萄糖引起二种不同状态下ＨｅｐＧ２ 细胞膜ＰＫＣ活性二相增高，胞浆ＰＫＣ 活性增高（ＮＤＲＨｅｐＧ２ 细胞） 或降低（ＤＲＨｅｐＧ２ 细胞）（ Ｐ＜ ０ ．０１） 。１０－ ７ ｍｏｌ／Ｌ胰岛素和２５ ｍ ｍｏｌ／Ｌ葡萄糖同时刺激细胞，膜和胞浆ＰＫＣ活性的变化与２５ ｍ ｍｏｌ／Ｌ葡萄糖单独刺激时基本一致。结论　ＰＫＣ上调与ＤＲＨｅｐＧ２ 细胞的胰岛素抵抗状态有关。１０－ ７ ｍｏｌ／Ｌ胰岛素或２５ ｍ ｍｏｌ／Ｌ葡萄糖刺激二?Objective To study the effects of high concentrations of insulin and glucose on the protein kinase C (PKC) activities of HepG2 cells. Methods A model of receptor down regulated HepG2 (DR HepG2) cells with characteristics of insulin resistance was developed. The membrane and cytosolic PKC activities of NDR HepG2 cells and DR HepG2 cells stimulated by 10 -7 mol/L insulin and 25mmol/L glucose were measured. Results Without stimulation by 10 -7 mol/L insulin or 25mmol/L glucose, the PKC activities of membrane and cytosol of the DR HepG2 cells were higher thanthoseobservedinNDR HepG2cells (P<0.05). 10 -7 mol/L insulin induced biphasic increases of membrane PKC activities by NDR HepG2 cells and DR HepG2 cells (P<0.01), the initial increase being at 30 sec and the secondary at 5～10min. Meanwhile, the activities of cytosolic PKC reduced markedly. 25mmol/L glucose induced biphasic increases of the membrane PKC activities by NDR HepG2 cells and DR HepG2 cells (P<0.01). At the same time the activities of cytosolic PKC increased slightly by NDR HepG2 cells or decreased by DR HepG2 cells. The effects of 25mmol/L glucose were parallel to those when 10 -7 mol/L insulin and 25mmol/L glucose were treated simultaneously. Conclusion The up regulation of PKC may be related to the insulin resistance of DR HepG2 cells. 10 -7 mol/L insulin or 25mmol/L glucose induced biphasic increases of membrane PKC activities of NDR HepG2 cells and DR HepG2 cells. But the effects on cytosolic PKC were different. PKC may be activated through the glucose induced mechanisms mainly when insulin and glucose were treated simultaneously.

关 键 词：胰岛素 葡萄糖 HEPG2细胞 PKC 胰岛素抵抗 

分 类 号：R587.02[医药卫生—内分泌]