• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >TNF-alpha and insulin, alone and synergistically, induce plasminogen activator inhibitor-1 expression in adipocytes.
【24h】

TNF-alpha and insulin, alone and synergistically, induce plasminogen activator inhibitor-1 expression in adipocytes.

机译：TNF-α和胰岛素单独或协同诱导脂肪细胞中纤溶酶原激活物抑制剂1的表达。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Obesity is associated with hyperinsulinemia and elevated concentrations of tumor necrosis factor-alpha (TNF-alpha) in adipose tissue. TNF-alpha has been implicated as an inducer of the synthesis of plasminogen activator inhibitor-1 (PAI-1), the primary physiological inhibitor of fibrinolysis, mediated by plasminogen activators in cultured adipocytes. To identify mechanism(s) through which TNF-alpha induces PAI-1, 3T3-L1 preadipocytes were differentiated into adipocytes and exposed to TNF-alpha for 24 h. TNF-alpha selectively increased the synthesis of PAI-1 without increasing activity of plasminogen activators. Both superoxide (generated by xanthine oxidase plus hypoxanthine) and hydrogen peroxide were potent inducers of PAI-1, and hydroxyl radical scavengers completely abolished the TNF-alpha induction of PAI-1. Exposure of adipocytes to TNF-alpha or insulin alone over 5 days increased PAI-1 production. These agonists exert synergistic effects. Results obtained suggest that TNF-alpha stimulates PAI-1 production by adipocytes, an effect potentiated by insulin, and that adipocyte generation of reactive oxygen centered radicals mediates the induction of PAI-1 production by TNF-alpha. Because induction of PAI-1 by TNF-alpha is potentiated synergistically by insulin, both agonists appear likely to contribute to the impairment of fibrinolytic system capacity typical in obese, hyperinsulinemic patients.
机译：肥胖与高胰岛素血症和脂肪组织中肿瘤坏死因子-α（TNF-α）浓度升高有关。 TNF-α被认为是纤溶酶原激活物抑制剂1（PAI-1）的合成诱导剂，纤溶酶原激活物抑制剂1（PAI-1）是纤溶酶的主要生理抑制剂，由纤溶酶原激活物介导培养的脂肪细胞。为了确定TNF-α诱导PAI-1的机制，将3T3-L1前脂肪细胞分化为脂肪细胞，并暴露于TNF-α24小时。 TNF-α选择性增加PAI-1的合成，而不会增加纤溶酶原激活剂的活性。过氧化物（由黄嘌呤氧化酶加次黄嘌呤生成）和过氧化氢都是PAI-1的有效诱导剂，羟基自由基清除剂完全消除了PAI-1的TNF-α诱导作用。在5天之内，仅将脂肪细胞暴露于TNF-α或胰岛素会增加PAI-1的产生。这些激动剂发挥协同作用。获得的结果表明，TNF-α刺激脂肪细胞产生PAI-1，胰岛素增强了这种作用，并且脂肪细胞产生的以活性氧为中心的自由基介导了TNF-α诱导PAI-1产生。由于胰岛素可协同增强TNF-α对PAI-1的诱导作用，因此两种激动剂似乎都可能导致肥胖，高胰岛素血症患者典型的纤溶系统功能受损。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号