Light alcohol consumption has the potential to suppress hepatocellular injury and liver fibrosis in non-alcoholic fatty liver disease.

Kazutoshi Yamada,Rika Horii,Masao Honda,Eishiro Mizukoshi,Takuya Seike,Tatsuya Yamashita,Kuniaki Arai,Shuichi Kaneko,Masaaki Kitahara,Hajime Sunagozaka,Patricia Aspichueta

doi:10.1371/journal.pone.0191026

Abstract

Background & aimsThe modest consumption of alcohol has been reported to decrease the incidence of fatty liver or prevalence of steatohepatitis. In this study, we investigated the effect of light alcohol consumption on liver function and gene expression in patients with non-alcoholic fatty liver disease (NAFLD).MethodsThe study group was formed of 178 patients diagnosed with non-alcoholic fatty liver disease, subclassified into two groups for analysis based on the daily alcohol consumption: non-alcohol group and light alcohol consumer group (≤20 g of ethanol/day). Clinical characteristics, liver histological features, gene expression, comprehensively analyzed using microarrays (BRB-Array tools), and molecular network were evaluated and compared between the two groups.ResultsNo significant differences in steatosis or inflammation score were noted among the groups. However, the ballooning and fibrosis scores were significantly lower in the light alcohol consumer group than in the non-alcohol group. Gene expression analysis revealed a marked inhibition of the pathways involved in the immune response in the light alcohol group compared to that in the non-alcohol group.ConclusionsLight alcohol consumption might suppress activity of non-alcoholic steatohepatitis by reducing gene expression levels involved in the immune response. This inhibition in gene expression was associated with a lowering of liver fibrosis and hepatocellular injury.

Highlights

Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease, with non-alcoholic steatohepatitis (NASH) being identified in approximately 20% of cases of NAFLD [1, 2]
We investigated the effect of light alcohol consumption on liver function and gene expression in patients with non-alcoholic fatty liver disease (NAFLD)
Light alcohol consumption might suppress activity of non-alcoholic steatohepatitis by reducing gene expression levels involved in the immune response

Summary

Introduction

Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease, with non-alcoholic steatohepatitis (NASH) being identified in approximately 20% of cases of NAFLD [1, 2]. Alcohol consumption is considered an exacerbating factor of metabolic syndrome and liver disease, with the effects of alcohol being mediated through the association between alcohol consumption and a high-fat diet or obesity [5,6]. An epidemiological review of health status data for a general population has demonstrated that the prevalence of metabolic syndrome is lower in individuals with light to moderate alcohol consumption than in those who do not consume alcohol [7]. Other studies have reported a beneficial effect of modest alcohol intake in reducing the risk of a cardiovascular event [8]. The modest consumption of alcohol has been reported to decrease the incidence of fatty liver or prevalence of steatohepatitis. We investigated the effect of light alcohol consumption on liver function and gene expression in patients with non-alcoholic fatty liver disease (NAFLD)

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