Hepatitis B virus infection is not associated with fatty liver disease: Evidence from a cohort study and functional analysis

Wang,Bingqian; Li,Wenna; Fang,Hezhi; Zhou,Huaibin

doi:10.3892/mmr.2018.9619

Hepatitis B virus infection is not associated with fatty liver disease: Evidence from a cohort study and functional analysis

Authors:
- Bingqian Wang
- Wenna Li
- Hezhi Fang
- Huaibin Zhou
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Affiliations: Key Laboratory of Laboratory Medicine, Ministry of Education, Zhejiang Provincial Key Laboratory of Medical Genetics, College of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, P.R. China
Published online on: November 2, 2018 https://doi.org/10.3892/mmr.2018.9619
Pages: 320-326
Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Chronic hepatitis B virus (HBV) infection has been reported to be associated with the prevalence of non‑alcoholic fatty liver disease (NAFLD). However, the present study demonstrated that the incidence of fatty liver disease in HBV‑infected subjects (16/152, 10.5%) was not significantly different from in non‑HBV‑infected subjects (292/1,714, 17%), following adjustment for age (odds ratio=0.656; 95% confidence interval=0.379‑1.134; P=0.131). Hepatitis B protein X (HBx) is considered a key regulator in HBV infection and several studies have confirmed that HBx serves a pivotal role in the process of fatty liver disease. In the present study, it was demonstrated that HBx‑expressing cells exhibited increased mitochondrial membrane potential, ATP generation, and endogenous mitochondrial respiration. In addition, higher levels of mitochondrial reactive oxygen species (ROS) were detected in HBx‑expressing cells compared with in control cells. Increased ROS production may contribute to increased lipid droplet formation in HBx‑expressing cells, whereas the removal of ROS with N‑acetylcysteine may decrease the accumulation of lipid droplets in a time‑dependent manner. In conclusion, the present findings indicated that HBV, and perhaps more specifically HBx, was not a protective factor against NAFLD. HBx may function as a risk factor for fatty liver disease, based on the findings of the present functional study; however, further studies are required to clarify the effects of HBx on hepatic steatosis.

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