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17β雌二醇增强小鼠肌原细胞的胰岛素效应
引用本文:李峰,王文龙,田宗城,刘美莲,谢平,宋惠萍.17β雌二醇增强小鼠肌原细胞的胰岛素效应[J].中国病理生理杂志,2003,19(12):1653-1657.
作者姓名:李峰  王文龙  田宗城  刘美莲  谢平  宋惠萍
作者单位:1. 中南大学湘雅医学院瘤研究所, 湖南 长沙 410078;
2. 湖南文理学院生命科学系, 湖南 常德 415000;
3. 中南大学湘雅医学院生物化学教研室, 湖南 长沙 410078
摘    要:目的:探讨17β雌二醇对小鼠肌原细胞的胰岛素效应的影响和对高胰岛素诱导的胰岛素抵抗的防止作用。方法:将小鼠肌原细胞分为6组, 3组不加高胰岛素(5×10-7 mol/L)预处理24 h后, 以其中1组为对照, 另2组分别用1 nmol/L、10 nmol/L的17β雌二醇再处理24 h。另外3组加高胰岛素(5×10-7 mol/L)预处理24 h之后, 弃培养液, 用冷的PBS洗涤细胞3次, 即为胰岛素抵抗细胞, 以其中1组为胰岛素抵抗细胞组, 另2组分别用1 nmol/L、10 nmol/L的17β雌二醇再处理24 h。对上述6组细胞进行胰岛素刺激的葡萄糖摄取能力、糖原合酶(GS)、磷酸果糖激酶(PFK)和丙酮酸激酶(PK)的活性测定。结果:17β雌二醇可提高小鼠肌原细胞的葡萄糖转运能力;提高总糖原合酶活性和糖原合酶的活性;还可增强细胞的磷酸果糖激酶和丙酮酸激酶活性。 结论:17β雌二醇可加强小鼠肌原细胞的胰岛素效应和防止高胰岛素诱导的胰岛素抵抗。

关 键 词:肌原细胞  雌二醇  胰岛素  胰岛素抗药性  
文章编号:1000-4718(2003)12-1653-05
收稿时间:2002-09-04
修稿时间:2002年9月4日

Insulin action potentiation by 17β-estradiol in cultured C2C12 mytoblasts
LI Feng ,WANG Wen-long ,TIAN Zong-cheng ,LIU Mei-lian ,XIE Ping ,SONG Hui-ping.Insulin action potentiation by 17β-estradiol in cultured C2C12 mytoblasts[J].Chinese Journal of Pathophysiology,2003,19(12):1653-1657.
Authors:LI Feng    WANG Wen-long  TIAN Zong-cheng  LIU Mei-lian  XIE Ping  SONG Hui-ping
Institution:1. Cancer Research Institute, Central South University, Changsha 410078, China;
2. Department of Bioscience, Hunan University of Arts and Science, Changde 415000, China;
3. Department of Biochemistry, Xiangya School of Medicine, Central South University, Changsha 410078, China
Abstract:AIM:To investigate the effect of 17β-estradiol on insulin action in cultured C2C12 mytoblasts. METHODS:C2C12 mytoblasts were cultured in 35 mm wells of six-well culture plate in an atmosphere of 5% CO2 at 37℃ in DMEM supplemented with 10% FBS and penicillin/streptomycin(1×105 U/L) to reach 80% confluence. Insulin-resistance C2C12 mytoblasts were obtained by incubating the cells for 24 hours in the presence of a high concentration (5×10-7 mol/L) of insulin. After treatmented with 17β-estradiol (1 nmol/L and 10 nmol/L, respectively) for 24 hours, C2C12 mytoblasts were performed to measure insulin-stimulated 2-DG uptake and GS, PFK, PK activities. RESULTS:17β-estradiol enhanced the capacity of insulin-stimulited 2-DG uptake, increased the GS, PFK and PK activities and prevented insulin-induced resistance in cultured C2C12 mytoblasts. CONCLUSION:17β-estradiol potentiates insulin action and preventes insulin-induced resistance in cultured C2C12 mytoblasts.
Keywords:Mytoblasts  Estradiol  Insulin  Insulin resistance
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