Nonalcoholic fatty liver disease
Nonalcoholic fatty liver disease
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DOI：
10.1016/j.bpg.2010.08.005
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发表时间：
2010-10-01
影响因子：
3.2
通讯作者：
Portincasa, Piero
中科院分区：
文献类型：
--
作者：
Krawczyk, Marcin;Bonfrate, Leonilde;Portincasa, Piero
非酒精性脂肪性肝病（NAFLD）是西方世界最常见的肝脏疾病，是肝脏中甘油三酯过量积累的一种气候组织病理学实体。非酒精性脂肪性肝炎（NASH）是一种坏死炎症形式，可导致晚期肝纤维化、肝硬化和肝细胞癌。NAFLD/NASH的发病机制复杂，但内脏脂肪增加和胰岛素抵抗与游离脂肪酸释放增加有关肝脏中的其他事件包括氧化应激和脂质过氧化降低抗氧化防御早期线粒体功能障碍铁积累脂肪源性脂肪因子失衡慢性促炎状态和肠道微生物加合物新的基因多态性增加了脂肪肝的风险，即APOC3和PNPLA3最近被发现，从而进一步了解脂肪肝的发病机制在我们的综述中，NAFLD的病理、生理、遗传和基本诊断和治疗方面进行了研究，并强调了该领域的未来趋势(C) 2010 Elsevier Ltd版权所有
Non-alcoholic fatty liver disease (NAFLD) the most common liver disorder in the Western world is a climco-histopathological entity in which excessive triglyceride accumulation in the liver occurs Non-alcoholic steatohepatitis (NASH) represents the necroinflammatory form which can lead to advanced liver fibrosis cirrhosis and hepatocellular carcinoma The pathogenesis of NAFLD/NASH is complex but Increased visceral adiposity plus insulin resistance with increased free fatty acids release play an initial key role for the onset and perpetuation of liver steatosis Further events in the liver include oxidative stress and lipid peroxidation decreased antioxidant defences early mitochondrial dysfunction iron accumulation unbalance of adipose-derived adipokines with a chronic proinflammatory status and gut-derived microbial adducts New gene polymorphisms increasing the risk of fatty liver namely APOC3 and PNPLA3 have been lately identified allowing further insights into the pathogenesis of this condition In our review pathophysiological genetic, and essential diagnostic and therapeutic aspects of NAFLD are examined with future trends in this field highlighted (C) 2010 Elsevier Ltd All rights reserved