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

ABSTRACT: The 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).The 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.No 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.Light 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.

SUBMITTER: Yamada K

PROVIDER: S-EPMC5771612 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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

Yamada Kazutoshi K Mizukoshi Eishiro E Seike Takuya T Horii Rika R Kitahara Masaaki M Sunagozaka Hajime H Arai Kuniaki K Yamashita Tatsuya T Honda Masao M Kaneko Shuichi S

PloS one 20180117 1

<h4>Background & aims</h4>The 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).<h4>Methods</h4>The 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 ...[more]

PMID: 29342182

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Project description:The prevalence of nonalcoholic fatty liver disease (NAFLD) is estimated to be 26.3% among the US population. A subset of this population exhibits an aggressive histological phenotype, nonalcoholic steatohepatitis (NASH) with ? stage 2 fibrosis, which may progress to cirrhosis. The definition of NAFLD excludes excessive alcohol intake, which is well known to cause alcoholic liver disease and will not be discussed here. Most NAFLD clinical trials use ~14 drinks per week as the cutoff for excessive alcohol intake. Alcohol consumption below this threshold, which we define as moderate alcohol consumption, is common in the US. According to the 2012 Behavioral Risk Factor Surveillance System (BRFSS), 56% of the US adult population consume alcohol, but only 8.2% report drinking heavily and 18.3% report binge drinking. The American Association for the Study of Liver Diseases (AASLD) Practice Guidance of 2018 states that there are insufficient data to make a recommendation with regard to moderate alcohol consumption in patients with NAFLD, citing a lack of longitudinal studies that examine the impact of moderate alcohol consumption on disease progression and its extrahepatic harms versus benefits, specifically in individuals with established NAFLD. NAFLD prevalence studies have generally noted a negative correlation between modest alcohol consumption and NAFLD. However, prevalence studies have limited application to patients with established NAFLD who present to the clinic. There can also be many confounding factors, because modest alcohol consumption is also negatively associated with some NAFLD risk factors, and those risk factors may not be adequately adjusted for in analyses. The prevalence of NASH with significant fibrosis (? F2) is more important because this is the group that is believed to have progressive disease. Thus, cohort studies of disease progression are more important from the patient's standpoint. Because these patients have already developed NAFLD or NASH, their interest lies in their odds of disease progression if they have moderate alcohol consumption compared to abstinence. It is also noteworthy that cardiovascular disease is the most important cause of death among patients with NAFLD. Moderate alcohol consumption has been associated with a reduction in overall mortality, but mostly in cardiovascular mortality. However, this protective effect has not been demonstrated specifically in patients with NAFLD.

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

Publications

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

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