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

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.

Chronic moderate alcohol consumption relieves high‐fat high‐cholesterol diet‐induced liver fibrosis in a rat model

“…Long‐term heavy drinking can cause alcoholic liver disease with or without NAFLD. An increasing number of clinical studies have shown that chronic moderate alcohol consumption produces beneficial effects on the low incidence of fatty liver in population and improvement of NAFLD in histology . These results need to be proven in murine models.…”

“…Kwon found that regular alcohol consumption over the course of a lifetime compared to minimal intake appears to have a protective effect on the histological severity of liver disease among patients with NAFLD . Similarly, Yamada et al found that the ballooning and fibrosis scores were significantly lower in NAFLD patients with light alcohol consumption (≤ 20 g of ethanol/d) than in non‐alcohol patients …”

Letter to the Editor: Moderate Alcohol Use in Fatty Liver Disease: Don’t Throw the Cabernet Out With the Bathwater

“…In a previous large cohort study, wine consumption up to 10 g/day reduced the risk of hepatic steatosis by 50% . A case‐control study examining histology and gene array also found that low‐level alcohol may suppress gene expression involved in the immune response that drives steatohepatitis . Given the small numbers of patients in the current study reporting low‐level wine consumption, it was likely underpowered to assess benefit.…”

Screening and functional analysis of differentially expressed genes in an animal model ofEBV-associated lymphomas

“…Based on this previous work, gene expression profiles in lymphoma cells and the corresponding normal donor PBLs were detected in the present study by high-throughput whole genome expression microarray. Differential expressed genes were analyzed using SAM [14], BRB [15] and LIMMA [16], which identified a total of 202 significantly differentially expressed genes, comprising 44 up-regulated genes and 158 down-regulated genes in the EBV-induced lymphomas.…”

“…Differential gene expression was determined using three methods, namely significance analysis of microarrays (SAM) [14], Biometric Research Program (BRB) [15], and Linear Models for Microarray and RNA-Seq analysis (LIMMA) [16], to ensure that the genes were significantly differentially expressed (differential expression indicated by all three methods). The threshold value for all three methods was set at 2fold change and a false discovery rate of <0.001.…”