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高脂饮食诱导的 microRNA-467b 下调增加了肝脂肪变性中的脂蛋白脂肪酶。

High fat diet induced downregulation of microRNA-467b increased lipoprotein lipase in hepatic steatosis.

机构信息

Functional Food Research Center, Research Division for Emerging Innovative Technology, Korea Food Research Institute, Seoungnam-si, Gyeonggi-do 463-746, South Korea.

出版信息

Biochem Biophys Res Commun. 2011 Nov 4;414(4):664-9. doi: 10.1016/j.bbrc.2011.09.120. Epub 2011 Oct 1.

DOI:10.1016/j.bbrc.2011.09.120
PMID:21986524
Abstract

Non-alcoholic fatty liver disease (NAFLD) is characterized by hepatic fat accumulation and is presently the most common chronic liver disease. However, the mechanisms underlying the development of steatosis remain unclear. MicroRNAs (miRNAs) are small non-coding RNAs that modulate a variety of biological functions. We have investigated the role of miRNA in the development of steatosis. We found that miR-467b expression is significantly downregulated in liver tissues of high-fat diet fed mice and in steatosis-induced hepatocytes. The downregulation of miR-467b resulted in the upregulation of hepatic lipoprotein lipase (LPL), the direct target of miR-467b. Moreover, the interaction between miR-467b and LPL was associated with insulin resistance, a major cause of NAFLD. These results suggest that downregulation of miR-467b is involved in the development of hepatic steatosis by modulating the expression of its target, LPL.

摘要

非酒精性脂肪性肝病(NAFLD)的特征是肝脂肪堆积,目前是最常见的慢性肝病。然而,脂肪变性发展的机制仍不清楚。微小 RNA(miRNA)是一种调节多种生物学功能的小非编码 RNA。我们研究了 miRNA 在脂肪变性发展中的作用。我们发现,高脂饮食喂养的小鼠肝组织和脂肪变性诱导的肝细胞中 miR-467b 的表达显著下调。miR-467b 的下调导致其直接靶标肝脂蛋白脂肪酶(LPL)的上调。此外,miR-467b 与 LPL 之间的相互作用与胰岛素抵抗有关,这是 NAFLD 的主要原因。这些结果表明,miR-467b 的下调通过调节其靶标 LPL 的表达参与肝脂肪变性的发展。

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