乙型肝炎病毒通过乙型肝炎核心蛋白增加酒精性脂肪肝的肝

StephenW

J Lipid Res. 2017 Nov 13. pii: jlr.M079533. doi: 10.1194/jlr.M079533. [Epub ahead of print]
Intracellular hepatitis B virus increases hepatic cholesterol deposition in alcoholic fatty liver via hepatitis B core protein.Wang YQ1, Wu T1, Hu DQ1, Weng XX1, Wang XJ1, Chen PJ2, Luo XP1, Wang HW1, Ning Q3.
Author information
1Tongji Hospital, China.2National Taiwan University, Taiwan.3Tongji Hospital, China; [email protected].

AbstractHepatits B virus (HBV) infection is a prevalent infectious disease with serious outcomes like chronic and acute hepatitis, cirrhosis and hepatocellular carcinoma. However, the metabolic alteration by HBV is rarely taken into concerns. With the high prevalence of alcohol consumption and chronic HBV infection, their overlap is assumed as an increasing latent hazard although without exact calculation, moreover, the impact of chronic alcoholic consumption combined with HBV on cholesterol metabolism is unknown. Six-week-old male FVB/Ncrl mice were hydrodynamically injected with a pGEM-4Z-1.3HBV vector and then fed with an ethanol diet for 6 weeks. Serum biomarkers and liver histology, liver cholesterol levels, and cholesterol metabolism-related molecules were measured. In vitro assay with HBx, HBs or HBc protein expression in HepG2 cells and co-stimulated with ethanol was conducted to assess the cholesterol metabolism. HBV expression synergistically increased cholesterol deposition in the setting of alcoholic fatty liver. The increase of intrahepatic cholesterol was succumbed to metabolic alteration in cholesterol metabolism including increased cholesterol synthesis, decreased cholesterol degradation, impaired cholesterol uptake. Ectopic expression of HBV component HBc, but not HBs and HBx, selectively promotes hepatocelluar cholesterol level.

Copyright © 2017, The American Society for Biochemistry and Molecular Biology.

KEYWORDS: Alcohol liver disease; Cholesterol; Cholesterol/Biosynthesis; Cholesterol/Cell and tissue; Cholesterol/Metabolism; Hepatitis B virus; Liver

PMID:29133292DOI:10.1194/jlr.M079533

StephenW

J Lipid Res。 2017年11月13日，pii：jlr.M079533。 doi：10.1194 / jlr.M079533。 [电子版提前打印]
乙型肝炎病毒通过乙型肝炎核心蛋白增加酒精性脂肪肝的肝脏胆固醇沉积。
王Q琦吴梧Hu胡德琦翁XX1王小军陈丕杰罗XP XP1王维宁宁Q3
作者信息

1
    中国同济医院。
2
    台湾大学台湾
3
    中国同济医院; [email protected]。

抽象

乙型肝炎病毒（HBV）感染是一种流行的传染病，其严重后果如慢性和急性肝炎，肝硬化和肝细胞癌。然而，HBV的代谢改变很少受到关注。由于酒精摄入量和慢性HBV感染的高发病率，尽管没有准确的计算，它们的重叠被认为是潜在的危险增加，而且慢性酒精消费与HBV联合对胆固醇代谢的影响还不清楚。 6周龄的雄性FVB / Ncrl小鼠用pGEM-4Z-1.3HBV载体进行流体动力学注射，然后用乙醇饮食喂养6周。测量血清生物标志物和肝脏组织学，肝脏胆固醇水平和胆固醇代谢相关分子。用HBx，HBs或HBc蛋白在HepG2细胞中表达并用乙醇共刺激进行体外测定来评估胆固醇代谢。乙型肝炎病毒表达协同增加胆固醇沉积在酒精性脂肪肝的设置。肝内胆固醇的增加导致胆固醇代谢的代谢改变，包括胆固醇合成增加，胆固醇降低减少，胆固醇摄取受损。 HBV组分HBc的异位表达，而不是HBs和HBx，选择性地促进肝细胞胆固醇水平。

版权©2017，美国生物化学与分子生物学学会。
关键词：

酒精肝病;胆固醇;胆固醇/生物合成;胆固醇/细胞和组织;胆固醇/代谢;乙型肝炎病毒;肝

结论：
    29133292
DOI：
    10.1194 / jlr.M079533