非酒精性脂肪性肝病和脂肪性肝炎小鼠模型。

ISRN hepatology Pub Date : 2012-12-12 eCollection Date: 2013-01-01 DOI:10.1155/2013/237870
Masashi Ninomiya, Yasuteru Kondo, Tooru Shimosegawa
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引用次数: 6

摘要

1980年,Ludwig等人首次报道了脂肪性肝炎患者,他们没有过度饮酒史,但肝脏组织学与酒精性肝炎相似,并进展为肝硬化,伴有炎症和纤维化。非酒精性脂肪性肝炎(NASH)的发展与肥胖、糖尿病、胰岛素抵抗和高脂血症有关。然而,NASH的发病机制仍不完整。基于动物模型提出了NASH发病机制的“多重打击”假说,这仍然是该领域研究的基础。我们回顾了重要的饮食和遗传动物模型,并讨论了NASH的发病机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Murine Models of Nonalcoholic Fatty Liver Disease and Steatohepatitis.

In 1980, Ludwig et al. first reported patients of steatohepatitis who lacked a history of excessive alcohol consumption but showed liver histology resembling alcoholic hepatitis and progression to cirrhosis of the liver accompanied by inflammation and fibrosis. The development of nonalcoholic steatohepatitis (NASH) is associated with obesity, diabetes mellitus, insulin resistance, and hyperlipidemia. However, the pathogenesis of NASH remains incomplete. A "multiple-hit" hypothesis for the pathogenesis of NASH based on an animal model has been proposed and remains a foundation for research in this field. We review the important dietary and genetic animal models and discuss the pathogenesis of NASH.

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