Pathogenesis of steatohepatitis
Pathogenesis of steatohepatitis
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DOI：
10.1053/bega.2002.0333
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发表时间：
2002-10-01
影响因子：
3.2
通讯作者：
Day, CP
中科院分区：
文献类型：
--
作者：
Day, CP
了解非酒精性脂肪性肝炎的发病机制，最近承担了非常重要的认识，它有可能进展到纤维化和肝硬化。1998年提出了发病机制的“两次打击”模型，第一次“打击”-脂肪变性增加了肝脏对第二次“打击”介导肝损伤的敏感性。本章的主要目的是根据随后4年中发表的研究报告对这一模式进行审查。特别注意将集中在胰岛素抵抗的作用和最近的进展，我们的理解的基本细胞机制联系肥胖和胰岛素抵抗。基于这些信息，我将提出一个修改的两个打击模型，更加强调的作用，游离脂肪酸。该模型将为进一步的研究提供基础，并使治疗策略的合理设计成为可能。
Understanding the pathogenesis of non-alcoholic steatohepatitis has recently assumed great importance with the recognition that it has the potential to progress to fibrosis and cirrhosis. The 'two-hit' model of pathogenesis was proposed in 1998, with the first 'hit' - steatosis increasing the sensitivity of the liver to the second 'hits' mediating liver injury. The main aim of this chapter is to review this model in the light of studies that have been published over the subsequent 4 years. Particular attention will be focused on the role of insulin resistance and recent advances in our understanding of the basic cellular mechanisms linking obesity and insulin resistance. Based on this information I will propose a modification of the two-hit model that places more emphasis on the role of free fatty acids. This model will provide the basis for further research and enable the rational design of treatment strategies.