The liver is an important target for ethanol induced DNA methylation changes that affect normal physiological function. Chronic ethanol consumption leads to abnormal regulation of the methylation pathway by inhibiting methionine adenosyl transferase the enzyme that converts methionine to SAM. This enzymatic inhibition leads to global DNA hypomethylation (French, 2013; Varela-Rey, Woodhoo, Martinez-Chantar, Mato, & Lu, 2013). Methylation patterns can also be affected by altered DNMT activity. For example, alcoholic patients have lower expression levels of DNMT3b (Bonsch et al., 2006) and acetaldehyde, the breakdown product of alcohol, which has been shown to inhibit DNMT activity (Garro, McBeth, Lima, & Lieber, 1991). Ethanol-induced hepatic steatosis (fatty liver) was reduced in DNMT1 hypomorphic mice suggesting a role for DNMTs in the progression of hepatic liver disease (Kutay et al., 2012). The effects of alcohol on methylation patterns have been implicated in advanced disease states such as alcoholic liver disease and cancer and further research may therefore provide promising therapeutic targets for pharmacological intervention (Varela-Rey et al., 2013).
