Alcoholic liver disease (ALD) occurs on a spectrum of severity. The majority of people who drink excessively develop a fatty liver, which though often symptom free, can progress to a state of inflammation, fibrosis, and cell death that can be fatal. Little is known about liver disruption that may occur in problem drinkers who are not alcohol dependent. To help understand the development of ALD, this study used a rodent model to examine differences in liver damage between binge drinkers and heavy drinkers.

Researchers at UCSF compared the metabolic effects in mice of repeated binge-like alcohol drinking, a single binge-drinking session, and repeated moderate alcohol drinking. Several markers of early- and later-stage liver disruption were examined.

Results indicated that even limited binge-like alcohol drinking disrupts liver function, which could lead to more severe forms of liver damage. These findings point to several aspects of early liver dysfunction seen in humans, including fatty liver, induction of the liver metabolic enzyme CYP2E1, and increased alcohol metabolism. The study, funded by the NIH/NIAAA, also demonstrates the great potential value of preclinical studies for understanding human disorders.