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Am J Physiol Gastrointest Liver Physiol 280: G1178-G1186, 2001;
0193-1857/01 $5.00
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Vol. 280, Issue 6, G1178-G1186, June 2001

Development of an animal model of chronic alcohol-induced pancreatitis in the rat

Hiroshi Kono1, Mikio Nakagami1, Ivan Rusyn1,2, Henry D. Connor1, Branko Stefanovic3, David A. Brenner3, Ronald P. Mason2,4, Gavin E. Arteel1, and Ronald G. Thurman1,2

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 alpha 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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