Abstract
The variety of animal models used in the study of alcoholic liver disease reflects the formidable task of developing a model that replicates the human disease. We show that oral feeding of fatty acids derived from fish oil and ethanol induces fatty liver, necrosis, inflammation, and fibrosis. Together with the study of oxidative and nitrosative stress markers, cytokines, proteasome function, and protein studies, this model has provided an inexpensive and technically simple method of establishing pathological alcoholic liver injury.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Administration, Oral
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Alanine Transaminase / blood
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Alcohol Drinking / genetics
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Alcohol Drinking / metabolism
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Alcohol Drinking / pathology*
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Animals
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Blotting, Western
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Central Nervous System Depressants / administration & dosage
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Central Nervous System Depressants / metabolism
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Chymotrypsin / metabolism
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Cytochrome P-450 CYP2E1 / metabolism
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Dinoprost / analogs & derivatives
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Dinoprost / blood
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Disease Models, Animal*
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Electrophoretic Mobility Shift Assay
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Endotoxins / blood
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Ethanol / administration & dosage
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Ethanol / metabolism
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Fatty Acids / administration & dosage
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Fatty Liver, Alcoholic / pathology
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Female
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Immunohistochemistry
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Liver / enzymology
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Liver / pathology*
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Liver Diseases, Alcoholic / genetics
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Liver Diseases, Alcoholic / metabolism
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Liver Diseases, Alcoholic / pathology*
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Oxidative Stress
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Rats
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Rats, Wistar
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Reverse Transcriptase Polymerase Chain Reaction
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Self Administration
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Specimen Handling
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Staining and Labeling
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Thiobarbituric Acid Reactive Substances / metabolism
Substances
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Central Nervous System Depressants
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Endotoxins
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Fatty Acids
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Thiobarbituric Acid Reactive Substances
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8-epi-prostaglandin F2alpha
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Ethanol
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Dinoprost
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Cytochrome P-450 CYP2E1
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Alanine Transaminase
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Chymotrypsin