The Hepatitis B Virus X Protein Inhibits Secretion of Apolipoprotein B by Enhancing the Expression of N-Acetylglucosaminyltransferase III

Kang, Sung Koo; Chung, Tae‐Wook; Lee, Ji Young; Lee, Young Choon; Morton, Richard E.; Kim, Cheorl Ho

doi:10.1074/jbc.m403176200

Cited by 76 publications

(64 citation statements)

References 49 publications

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“…In addition, a lower serum TG level, as frequently seen in subjects free of hepatitis B infection, may also suggest that hepatic triglyceride accumulation, caused by hepatitis B X protein, originated from the hepatitis B genome. 30 It may have a strong influence on the secretion of apoB, which is associated with the development of liver cancer.…”

Section: Obesitymentioning

confidence: 99%

A population-based study investigating the association between metabolic syndrome and Hepatitis B/C infection (Keelung Community-based Integrated Screening Study No. 10)

et al. 2006

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Objectives: We aimed to assess the association between metabolic syndrome (MS) and hepatitis B/C virus infection using a large population-based study. Design and methods: A population-based cross-sectional study design was adopted with a total of 53 528 subjects being enrolled from the integrated multiple diseases screening program in Keelung, Taiwan. Evidence of past hepatitis B/C infection, acquired during childhood or as a young adult, was identified during the two-stage liver cancer screening part of the process. Information on biochemical markers and anthropometric measures related to MS, such as fasting blood sugar, triglyceride and high-density lipoprotein (HDL), abdominal circumference and blood pressure (BP), were collected routinely while screening for hypertension, type 2 diabetes, and hyperlipidemia. Logistic regression was used to estimate odds ratios and related 95% confidence intervals for the associations between MS and hepatitis B/C infection. Results: High blood pressure (SBPX135 mmHg or DBPX85 mmHg) (adjusted odd ratio: 0.89 (0.83-0.94)) and high triglyceride (X150 mg/dl) (adjusted odds ratio: 0.65 (0.60-0.69)) were, after adjusting for gender and age, inversely associated with being HBsAg positive (Po0.05). The likelihood of developing MS was lower in the HBsAg positive than the HBsAg negative (adjusted odds ratio: 0.84 (0.76-0.93)). A positive association between being anti-HCV positive and having low serum HDL (male o40 mg/dl, female o50 mg/dl) was also noted (adjusted odds ratio: 1.61 (1.37-1.88) after controlling for gender and age). High triglyceride was inversely associated with being anti-HCV positive (adjusted odds ratio: 0.63 (0.55-0.71). Conclusions: There is an inverse association between MS and hepatitis B virus infection whereas the association was heterogeneous for HCV infection with a positive association with abnormal serum HDL but an inverse association with hypertriglyceridemia.

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Section: Obesitymentioning

confidence: 99%

A population-based study investigating the association between metabolic syndrome and Hepatitis B/C infection (Keelung Community-based Integrated Screening Study No. 10)

et al. 2006

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“…Apolipoprotein B (apoB) in the liver is an important glycoprotein for transport of VLDL and low density lipoproteins (LDL). In liver cells hyper-express of HBx causes negative accommodation of microsome TG transfer protein, could increase the expression of β-d-mannoside-1, 4-N-acetylglucosaminyl transferase-III (GnT-III), and causes inhibition of apoB secretion and accumulation of intracellular TG and cholesterol (Tch) (Kang et al, 2004), but serum TG level in liver cancer did not obviously decrease compared with lipoprotein(a) (Lp(a)), Tch and HDL (Ooi et al, 2005).…”

Section: Influence Of Liver Cancer On Tg Me-tabolismmentioning

confidence: 99%

Lipids changes in liver cancer

Jiang

Zhang

et al. 2007

J. Zhejiang Univ. - Sci. B

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Abstract:Liver is one of the most important organs in energy metabolism. Most plasma apolipoproteins and endogenous lipids and lipoproteins are synthesized in the liver. It depends on the integrity of liver cellular function, which ensures homeostasis of lipid and lipoprotein metabolism. When liver cancer occurs, these processes are impaired and the plasma lipid and lipoprotein patterns may be changed. Liver cancer is the fifth common malignant tumor worldwide, and is closely related to the infections of hepatitis B virus (HBV) and hepatitis C virus (HCV). HBV and HCV infections are quite common in China and other Southeast Asian countries. In addition, liver cancer is often followed by a procession of chronic hepatitis or cirrhosis, so that hepatic function is damaged obviously on these bases, which may significantly influence lipid and lipoprotein metabolism in vivo. In this review we summarize the clinical significance of lipid and lipoprotein metabolism under liver cancer.

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“…The frequency of hepatic steatosis in subjects with a chronic HBV infection ranges from 27 to 51% (4). Furthermore, HBV X protein (HBx) is known to cause hepatic lipid deposition by inhibiting the secretion of apolipoprotein B (5). A previous report showed that the increased HBx expression can cause lipid accumulation in hepatocytes, likely mediated by sterol regulatory element binding protein 1 and peroxisome proliferator-activated receptor ␥ (PPAR␥) (4).…”

mentioning

confidence: 99%

Hepatitis B Virus X Protein Induces Hepatic Steatosis by Enhancing the Expression of Liver Fatty Acid Binding Protein

Peng

Zhu

et al. 2016

J Virol

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Hepatitis B virus (HBV) has been implicated as a potential trigger of hepatic steatosis although molecular mechanisms involved in the pathogenesis of HBV-associated hepatic steatosis still remain elusive. Our prior work has revealed that the expression level of liver fatty acid binding protein 1 (FABP1), a key regulator of hepatic lipid metabolism, was elevated in HBV-producing hepatoma cells. In this study, the effects of HBV X protein (HBx) mediated FABP1 regulation on hepatic steatosis and the underlying mechanism were determined. mRNA and protein levels of FABP1 were measured by quantitative RT-PCR (qPCR) and Western blotting. HBx-mediated FABP1 regulation was evaluated by luciferase assay, coimmunoprecipitation, and chromatin immunoprecipitation. Hepatic lipid accumulation was measured by using Oil-Red-O staining and the triglyceride level. It was found that expression of FABP1 was increased in HBV-producing hepatoma cells, the sera of HBV-infected patients, and the sera and liver tissues of HBV-transgenic mice. IMPORTANCEAccumulating evidence from epidemiological and experimental studies has indicated that chronic HBV infection is associated with hepatic steatosis. However, the molecular mechanism underlying HBV-induced pathogenesis of hepatic steatosis still remains to be elucidated. In this study, we found that expression of liver fatty acid binding protein (FABP1) was dramatically increased in the sera of HBV-infected patients and in both sera and liver tissues of HBV-transgenic mice. Forced expression of HBx led to FABP1 upregulation, whereas knockdown of FABP1 remarkably diminished lipid accumulation in both in vitro and in vivo models. It is possible that HBx promotes hepatic lipid accumulation through upregulating FABP1 in the development of HBV-induced nonalcoholic fatty liver disease. Therefore, inhibition of FABP1 might have therapeutic value in steatosis-associated chronic HBV infection. H epatitis B virus (HBV) infection is a serious health problemworldwide, causing acute and chronic hepatitis, cirrhosis, and hepatocellular carcinoma (1). Emerging evidence from epidemiological and experimental studies suggests that chronic HBV infection, as well as HCV infection, is associated with hepatic steatosis (2, 3). The frequency of hepatic steatosis in subjects with a chronic HBV infection ranges from 27 to 51% (4). Furthermore, HBV X protein (HBx) is known to cause hepatic lipid deposition by inhibiting the secretion of apolipoprotein B (5). A previous report showed that the increased HBx expression can cause lipid accumulation in hepatocytes, likely mediated by sterol regulatory element binding protein 1 and peroxisome proliferator-activated receptor ␥ (PPAR␥) (4). The molecular mechanism by which HBV induces the pathogenesis of hepatic steatosis remains elusive. Using fluorescent two-dimensional difference gel electrophoresis and matrix-assisted laser desorption ionization-time of flight mass spectrometry analysis, we found that the protein level of liver fatty acid binding protein (L-FABP ...

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The Hepatitis B Virus X Protein Inhibits Secretion of Apolipoprotein B by Enhancing the Expression of N-Acetylglucosaminyltransferase III

Cited by 76 publications

References 49 publications

A population-based study investigating the association between metabolic syndrome and Hepatitis B/C infection (Keelung Community-based Integrated Screening Study No. 10)

A population-based study investigating the association between metabolic syndrome and Hepatitis B/C infection (Keelung Community-based Integrated Screening Study No. 10)

Lipids changes in liver cancer

Hepatitis B Virus X Protein Induces Hepatic Steatosis by Enhancing the Expression of Liver Fatty Acid Binding Protein

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