Nonalcoholic fatty liver disease: molecular mechanisms for the hepatic steatosis.
Nonalcoholic fatty liver disease: molecular mechanisms for the hepatic steatosis.
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DOI：
10.3350/cmh.2013.19.3.210
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发表时间：
2013-09
影响因子：
8.9
通讯作者：
Koo SH
中科院分区：
文献类型：
--
作者：
Koo SH
肝脏在葡萄糖、脂肪酸和胆固醇等主要代谢物的生物生成中起着核心作用。现代社会肥胖发病率的增加促进了人类外周组织的胰岛素抵抗，并可通过诱导肝脏脂质积累引起严重的代谢紊乱，从而导致非酒精性脂肪性肝病（NAFLD）的进展。NAFLD以肝脏脂肪堆积增加为特征，可能先于更严重的疾病，如非酒精性脂肪性肝炎（NASH）、肝硬化和某些情况下的肝细胞癌。脂质在肝脏中的积累可以通过肝脏对游离脂肪酸的吸收增加、脂肪酸β氧化受损或新生脂肪生成发生率增加来追踪。在这篇综述中，我想把重点放在促进肝脂肪变性作为NAFLD前兆的个体途径的作用上。
Liver plays a central role in the biogenesis of major metabolites including glucose, fatty acids, and cholesterol. Increased incidence of obesity in the modern society promotes insulin resistance in the peripheral tissues in humans, and could cause severe metabolic disorders by inducing accumulation of lipid in the liver, resulting in the progression of non-alcoholic fatty liver disease (NAFLD). NAFLD, which is characterized by increased fat depots in the liver, could precede more severe diseases such as non-alcoholic steatohepatitis (NASH), cirrhosis, and in some cases hepatocellular carcinoma. Accumulation of lipid in the liver can be traced by increased uptake of free fatty acids into the liver, impaired fatty acid beta oxidation, or the increased incidence of de novo lipogenesis. In this review, I would like to focus on the roles of individual pathways that contribute to the hepatic steatosis as a precursor for the NAFLD.