Chronic alcohol consumption is a leading cause of chronic liver disease worldwide, leading to cirrhosis and hepatocellular carcinoma. Currently, the most widely used model for alcoholic liver injury is ad libitum feeding with the Lieber-DeCarli liquid diet containing ethanol for 4-6 weeks; however, this model, without the addition of a secondary insult, only induces mild steatosis, slight elevation of serum alanine transaminase (ALT) and little or no inflammation. Here we describe a simple mouse model of alcoholic liver injury by chronic ethanol feeding (10-d ad libitum oral feeding with the Lieber-DeCarli ethanol liquid diet) plus a single binge ethanol feeding. This protocol for chronic-plus-single-binge ethanol feeding synergistically induces liver injury, inflammation and fatty liver, which mimics acute-on-chronic alcoholic liver injury in patients. This feeding protocol can also be extended to chronic feeding for longer periods of time up to 8 weeks plus single or multiple binges. Chronic-binge ethanol feeding leads to high blood alcohol levels; thus, this simple model will be very useful for the study of alcoholic liver disease (ALD) and of other organs damaged by alcohol consumption.
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http://dx.doi.org/10.1038/nprot.2013.032 | DOI Listing |
Life Sci
January 2025
Department of Hepatobiliary Surgery, Jintan Affiliated Hospital of Jiangsu University, Changzhou, China. Electronic address:
Aims: Alcoholic liver disease (ALD) is characterized by aberrant lipid metabolism and chronic inflammation that eventually give rise to cirrhosis and hepatocellular carcinoma. In the present study we investigated the contribution of CC motif chemokine ligand 11 (CCL11) to ALD pathogenesis.
Methods And Materials: ALD was induced in mice by binge ethanol gavage or chronic ethanol feeding.
Stress is central to many neuropsychiatric conditions, including alcohol use disorder (AUD). Stress influences the initiation and continued use of alcohol, the progression to AUD, and relapse. Identifying the neurocircuits activated during stress, and individual variability in these responses is critical for developing new treatment targets for AUD, particularly to mitigate stress-induced relapse.
View Article and Find Full Text PDFHepatology
January 2025
Université Côte d'Azur, INSERM, U1065, C3M, Nice, France.
Background And Aims: Alcohol-related liver disease (ALD) is one of the leading causes of severe liver disease with limited pharmacological treatments for alcohol-related steatohepatitis (ASH). CD44, a glycoprotein mainly expressed in immune cells, has been implicated in multiple inflammatory diseases but has never been studied in the ALD context. We therefore studied its contribution to ASH development in mice and its expression in ALD patients.
View Article and Find Full Text PDFJ Environ Manage
January 2025
Department of Civil and Environmental Engineering, University of Illinois at Urbana-Champaign, Urbana, IL, 61801, USA. Electronic address:
As global phosphorus (P) stores rapidly decline, P fed algal blooms continue to threaten critical freshwater resources across the globe. In the Midwestern United States (US), particularly the Corn Belt, biorefineries could play a key role in addressing this issue. By recovering P from the byproducts of ethanol production these facilities could reduce the P content of distillers grain feed, thereby reducing P excreted in manures.
View Article and Find Full Text PDFBiomedicines
December 2024
Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA.
Susceptibility to and severity of pulmonary infections increase with ethanol consumption. We have previously shown that ethanol-induced changes in the gut microbiome disrupt gut homeostasis, allowing for the translocation of proinflammatory mediators into the circulation and eliciting an immune response in the lung. Additionally, targeting the gut with butyrate supplementation not only rescues ethanol-induced disruptions to gut health but also reverses aspects of immune dysregulation in the lungs.
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