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乙型肝炎和丙型肝炎与2型糖尿病的关系

覃超梅 刘永明 苏何玲

引用本文:
Citation:

乙型肝炎和丙型肝炎与2型糖尿病的关系

DOI: 10.3969/j.issn.1001-5256.2021.04.042
基金项目: 

国家自然科学基金项目 (81560341);

国家自然科学基金项目 (81460320);

广西自然科学基金资助项目 (2018GXNSFAA138153)

利益冲突声明:所有作者均不存在利益冲突。
作者贡献声明:覃超梅负责文献查阅、资料数据分析以及文章撰写;刘永明负责文字修改,并参与拟定写作思路;苏何玲负责拟定写作思路和指导撰写文章并最后定稿。
详细信息
    作者简介:

    覃超梅(1996—),女,主要从事HBV感染相关分子疾病研究

    通信作者:

    苏何玲,helingsu@glmc.edu.cn

  • 中图分类号: R512.6;R587.1

Association of hepatitis B and hepatitis C with type 2 diabetes mellitus

  • 摘要:

    乙型肝炎和丙型肝炎以及2型糖尿病(T2DM)均为全球性的严重公共卫生问题。分析了乙型和丙型肝炎与T2DM的关系。分析表明,一方面,乙型肝炎和丙型肝炎均促进T2DM发病,其发病机制涉及病毒感染抑制胰岛素信号转导和胰岛素靶细胞葡萄糖摄取以及糖原合成。另一方面,T2DM患者容易罹患乙型肝炎和丙型肝炎,这可能与糖尿病导致多种器官功能的破坏有关。

     

  • 图  1  HBV及HCV蛋白作用于胰岛素信号通路

    表  1  HBV作用于胰岛素信号途径相关因子

    HBV蛋白 胰岛素信号通路相关因子 机制 参考文献
    pre-S2 INSR 下调INSR基因启动子的活性,降低INSR的表达 [12-13]
    HBx IRS-1 HBx与前列腺六次跨膜蛋白2蛋白相互作用并降低其稳定性,阻止IRS-1蛋白降解 [14, 16]
    HBx Akt 激活肝细胞中的PI3K/Akt [15, 17]
    HBx GSK-3β 激活Akt并导致下游GSK-3β磷酸化,降低肝糖的合成 [18-19]
    HBx PDK1 上调PI3K的下游效应分子PDK1的表达 [20]
    下载: 导出CSV

    表  2  HCV作用于胰岛素信号途径相关因子

    HCV蛋白 胰岛素信号途径相关因子 机制 参考文献
    HCV core TNFα 上调TNFα,导致IRS-1/IRS-2的丝氨酸氨基酸磷酸化 [32]
    HCV core SOCS3 上调SOCS3,导致IRS-1/IRS-2降解 [33]
    HCV core GLUT2 下调GLUT2的细胞表达,从而抑制葡萄糖摄取 [44]
    下载: 导出CSV
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  • 收稿日期:  2020-11-10
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