The role of mitochondrial dysfunction in the pathogenesis of alcoholic liver disease has been long documented by multiple laboratories. The dietary supplementation with betaine protects against ethanol-induced loss in oxidative phosphorylation system proteins. Even if the exact mechanism for this protection at the organelle level is not known, betaine shows to preserve the function of the electron transport chain, to maintain the integrity of the liver, and to protect against the development of alcoholic liver injury by preventing NOS 2 induction and NO generation [67] . Moreover, specific changes are associated with the normalization of hepatic SAM : SAH ratio and maintenance of methylation potential in response to betaine supplementation during chronic ethanol ingestion.