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支链氨基酸在非酒精性脂肪性肝病发生发展中的作用

谢小青 刘亚贤 陈顺 于晓辉

引用本文:
Citation:

支链氨基酸在非酒精性脂肪性肝病发生发展中的作用

DOI: 10.3969/j.issn.1001-5256.2022.02.037
基金项目: 

甘肃省重点研发项目 (2020-0203-SFC-0242)

利益冲突声明:所有作者均声明不存在利益冲突。
作者贡献声明:谢小青负责课题设计,撰写论文;刘亚贤、陈顺参与修改论文;于晓辉负责拟定写作思路,指导撰写文章并最后定稿。
详细信息
    通信作者:

    于晓辉, yuxiaohui528@126.com

Role of branched-chain amino acids in the development and progression of nonalcoholic fatty liver disease

Research funding: 

Gansu Province Key R & D Projects (2020-0203-SFC-0242)

More Information
  • 摘要: 非酒精性脂肪性肝病是常见慢性肝病,有进展为非酒精性肝炎、肝纤维化和肝癌的风险,发病机制多样,其中支链氨基酸代谢异常可引起肝细胞氧化应激、自噬、线粒体功能障碍等,是导致非酒精性脂肪性肝病发生发展的最主要机制,对其进展进行综述,分析支链氨基酸代谢异常对非酒精性脂肪性肝病发生与发展的可能作用,以期提高临床认知与诊治水平。

     

  • 图  1  BCAA代谢与脂肪合成及代谢

    注:BCAA在BCAT的作用下生成相应的支链α-酮酸(BCKA),BCKA在BCKDH催化生成2-甲基酰CoA、异戊酰CoA、异丁酰CoA, 经一系列酶促反应生成乙酰CoA,最终进入TCA, 经过复合体Ⅰ(NADH)、Ⅱ、Ⅲ、Ⅳ氧化磷酸化后(OXPHOS)生成ATP和水。Cytc,细胞色素酶;Q,辅酶Q;HSL,激素敏感性脂肪酶;DHAP,3-磷酸甘油;HMG-CoA,羟甲基戊二酸单酰辅酶A;PGC-1α,过氧化物酶体增殖物激活受体-γ共激活因子1;Errα,雌激素相关受体α;Gabpα,GA结合蛋白α。

    图  2  BCAA与氧化应激及胰岛素抵抗信号通路

    注:S6K1,核糖体蛋白S6激酶1;GCN2,阻遏蛋白激酶2;JNK,c-Jun氨基末端激酶;IKK:kappaB激酶。

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  • 收稿日期:  2021-06-06
  • 录用日期:  2021-08-12
  • 出版日期:  2022-02-20
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