ArticleAlcoholism, clinical and experimental research2017
Limited Excessive Voluntary Alcohol Drinking Leads to Liver Dysfunction in Mice.
Article in Alcoholism, clinical and experimental research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Therapeutics for Alcohol-Associated Liver Disease.Annual review of pharmacology and toxicology · 2026Review
- Oxidative Stress and Alcohol-Related Hepatitis: A Role for Future Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- Operant ethanol self-administration behaviors do not predict sex differences in continuous access home cage drinking.Alcohol (Fayetteville, N.Y.) · 2025Article
- Impact of binge drinking on alcoholic liver disease.Archives of pharmacal research · 2025Review
- Sex- and estrous-related response patterns for alcohol depend critically on the level of compulsion-like challenge.Progress in neuro-psychopharmacology & biological psychiatry · 2024Article
- Engagement for alcohol escalates in the 5-choice serial reaction time task after intermittent access.Alcohol (Fayetteville, N.Y.) · 2024Article
- Independent and additive effects of binge drinking and obesity on liver enzymes: a cross-sectional analysis using the Korean National Health Insurance Service data.Gastroenterology report · 2024Article
- Preparation of Alcohol Dehydrogenase-Zinc Phosphate Hybrid Nanoflowers through Biomimetic Mineralization and Its Application in the Inhibitor Screening.Molecules (Basel, Switzerland) · 2023Article
- Article
- Adaptation of the 5-choice serial reaction time task to measure engagement and motivation for alcohol in mice.Frontiers in behavioral neuroscience · 2022Article
- Neuronal modulation of hepatic lipid accumulation induced by bingelike drinking.American journal of physiology. Endocrinology and metabolism · 2020Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundLiver damage is a serious and sometimes fatal consequence of long-term alcohol intake, which progresses from early-stage fatty liver (steatosis) to later-stage steatohepatitis with inflammation and fibrosis/necrosis. However, very little is known about earlier stages of liver disruption that may occur in problem drinkers, those who drink excessively but are not dependent on alcohol.
methodsWe examined how repeated binge-like alcohol drinking in C57BL/6 mice altered liver function, as compared with a single binge-intake session and with repeated moderate alcohol consumption. We measured a number of markers associated with early- and later-stage liver disruption, including liver steatosis, measures of liver cytochrome P4502E1 (CYP2E1) and alcohol dehydrogenase (ADH), alcohol metabolism, expression of cytokine mRNA, accumulation of 4-hydroxynonenal (4-HNE) as an indicator of oxidative stress, and alanine transaminase/aspartate transaminase as a measure of hepatocyte injury.
resultsImportantly, repeated binge-like alcohol drinking increased triglyceride levels in the liver and plasma, and increased lipid droplets in the liver, indicators of steatosis. In contrast, a single binge-intake session or repeated moderate alcohol consumption did not alter triglyceride levels. In addition, alcohol exposure can increase rates of alcohol metabolism through CYP2E1 and ADH, which can potentially increase oxidative stress and liver dysfunction. Intermittent, excessive alcohol intake increased liver CYP2E1 mRNA, protein, and activity, as well as ADH mRNA and activity. Furthermore, repeated, binge-like drinking, but not a single binge or moderate drinking, increased alcohol metabolism. Finally, repeated, excessive intake transiently elevated mRNA for the proinflammatory cytokine IL-1B and 4-HNE levels, but did not alter markers of later-stage liver hepatocyte injury.
conclusionsTogether, we provide data suggesting that even relatively limited binge-like alcohol drinking can lead to disruptions in liver function, which might facilitate the transition to more severe forms of liver damage.
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