Journal of hepatology · 1995
Ethanol-related liver injury in the rat: a model of steatosis, inflammation and pericentral fibrosis.
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Keegan A, Martini R, Batey R
Аннотация
BACKGROUND/AIMS: While several animal models exist for the study of ethanol heptotoxicity, they are limited in their applicability. This paper describes a relatively simple rat model of alcohol-related liver injury.
METHODS: Ethanol was supplied in the drinking water in a concentration of 40% v/v for up to 29 weeks. Animals are concurrently supplied a chow diet which provides adequate protein and choline for normal growth. Total fat intake is low (7% of consumed calories).
RESULTS: Histological changes of steatosis, inflammation, hepatocyte necrosis and pericentral sclerosis were evident in ethanol-treated rat livers. Littermate controls with and without pair-feeding had normal livers. Electron microscopy revealed abnormal mitochondria and a marked proliferation of smooth endoplasmic reticulum in livers of animals fed ethanol. Biochemical analysis revealed that levels of hepatic-free choline were similar in treated and pair-fed control rats. There was an expected increase in the activity of the microsomal enzyme cytochrome P450 2E1 in ethanol-fed rats.
CONCLUSIONS: The model provides a convenient method for the production of alcoholic liver injury, and it may be useful for the study of the pathogenesis of ethanol-related liver disease.
METHODS: Ethanol was supplied in the drinking water in a concentration of 40% v/v for up to 29 weeks. Animals are concurrently supplied a chow diet which provides adequate protein and choline for normal growth. Total fat intake is low (7% of consumed calories).
RESULTS: Histological changes of steatosis, inflammation, hepatocyte necrosis and pericentral sclerosis were evident in ethanol-treated rat livers. Littermate controls with and without pair-feeding had normal livers. Electron microscopy revealed abnormal mitochondria and a marked proliferation of smooth endoplasmic reticulum in livers of animals fed ethanol. Biochemical analysis revealed that levels of hepatic-free choline were similar in treated and pair-fed control rats. There was an expected increase in the activity of the microsomal enzyme cytochrome P450 2E1 in ethanol-fed rats.
CONCLUSIONS: The model provides a convenient method for the production of alcoholic liver injury, and it may be useful for the study of the pathogenesis of ethanol-related liver disease.