ArticleAlcohol, clinical & experimental research2025
Peripheral alcohol metabolism dictates ethanol consumption and drinking microstructure in mice.
Article in Alcohol, clinical & experimental research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed.
- Cued unpredictable intermittent access exacerbates loss of control over ethanol drinking.Neuropharmacology · 2026Article
- A ketogenic diet reduces hepatic alcohol metabolism and alcohol consumption in rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Cued unpredictable intermittent access exacerbates loss of control over ethanol drinking.bioRxiv : the preprint server for biology · 2026Article
- SqueakPose Studio, an end-to-end platform for pose estimation and real-time edge-AI deployment.eLife · 2026Article
- SqueakPose Studio: An end-to-end platform for pose estimation and real-time edge-AI deployment.bioRxiv : the preprint server for biology · 2026Article
- Cyp2e1 deletion in mice increases sensitivity to ethanol-induced motor impairment and escalation of drinking behavior in the chronic intermittent ethanol model.Alcohol, clinical & experimental research · 2025Article
- High-throughput quantitation of acetaldehyde and ethanol in mice using gas chromatography/mass spectrometry positive chemical ionization.Alcohol, clinical & experimental research · 2025Article
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Abstract
backgroundEthanol metabolism is intimately linked with the physiological and behavioral aspects of ethanol consumption. Ethanol is mainly oxidized by alcohol dehydrogenase (ADH) to acetaldehyde and further to acetate via aldehyde dehydrogenases (ALDHs). Understanding how ethanol and its metabolites work together to initiate and drive continued ethanol consumption is crucial for identifying interventions for alcohol use disorder (AUD). Therefore, the goal of our study was to determine how ADH1, which is mainly peripherally expressed and metabolizes >90% of ingested ethanol, modulates ethanol metabolite distribution and downstream behaviors.
methodsEthanol consumption in drinking-in-the-dark (DID) and two-bottle choice (2BC) drinking paradigms, ethanol metabolite concentrations, and lickometry were assessed after ADH1 inhibition and/or in Adh1-knockout (Adh1 KO) mice.
resultsWe found that Adh1 KO mice of both sexes exhibited decreased ethanol consumption and preference compared with wild-type (WT) mice in DID and 2BC. ADH1 inhibitor fomepizole (4-MP) also significantly decreased normal and sweetened ethanol consumption in DID studies. Measurement of ethanol and its metabolites revealed that ethanol was increased at 1 h but not 15 min, peripheral acetaldehyde was slightly decreased at both timepoints, and ethanol-induced increases in acetate were abolished after ethanol administration in Adh1 KO mice compared with controls. Similarly, ethanol accumulation as a function of consumption was 2-fold higher in Adh1 KO or 4-MP-treated mice compared with controls. We then used lickometry to determine how this perturbation in ethanol metabolism affects drinking microstructure. Adh1 KO mice consume most of their ethanol in the first 30 min, like WT mice, but display altered temporal shifts in drinking behaviors and do not form normal bout structures, resulting in lower ethanol consumption.
conclusionsOur study demonstrates that ADH1-mediated ethanol metabolism is a key determinant of ethanol consumption, highlighting a fundamental knowledge gap regarding how ethanol and its metabolites drive ethanol consumption.
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