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1 Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, 2 Curriculum in Toxicology, and 3 Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill 27599-7365; and 4 Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709
This study was designed to develop an animal model
of alcoholic pancreatitis and to test the hypothesis that the dose of
ethanol and the type of dietary fat affect free radical formation and pancreatic pathology. Female Wistar rats were fed liquid diets rich in
corn oil (unsaturated fat), with or without a standard or high dose of
ethanol, and medium-chain triglycerides (saturated fat) with a high
dose of ethanol for 8 wk enterally. The dose of ethanol was
increased as tolerance developed, which allowed approximately twice as
much alcohol to be delivered in the high-dose group. Serum pancreatic
enzymes and histology were normal after 4 wk of diets rich in
unsaturated fat, with or without the standard dose of ethanol. In
contrast, enzyme levels were elevated significantly by the high ethanol
dose. Increases were blunted significantly by dietary saturated fat.
Fibrosis and collagen 
1(I) expression in the pancreas were not
detectable after 4 wk of enteral ethanol feeding; however, they were
enhanced significantly by the high dose after 8 wk. Furthermore,
radical adducts detected by electron spin resonance were minimal with
the standard dose; however, the high dose increased carbon-centered
radical adducts as well as 4-hydroxynonenal, an index of lipid
peroxidation, significantly. Radical adducts were also blunted by
~70% by dietary saturated fat. The animal model presented here is
the first to demonstrate chronic alcohol-induced pancreatitis in a
reproducible manner. The key factors responsible for pathology are the
amount of ethanol administered and the type of dietary fat.
medium-chain triglycerides; fibrosis; free radical; enteral feeding
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