Ethanol-induced Steatosis Research Articles

Chronic ethanol feeding causes accumulation of serum cholesterol in rat pancreas

In a previous study, a rat model of ethanol-induced pancreatic steatosis was developed in which chronic ethanol feeding resulted in a twofold increase in pancreatic cholesteryl ester content. The studies reported here were performed in order to elucidate the mechanism of this cholesteryl ester accumulation. Rats were pair fed ethanol or control diets for 3 weeks. Ethanol feeding resulted in an increased accumulation of serum cholesterol in the pancreas. Ethanol feeding also resulted in increased in vitro incorporation of labeled acetate and mevalonate into the sterol moiety of pancreatic cholesteryl ester and increased incorporation of labeled acetate into its fatty acid component. These results suggest that chronic ethanol feeding causes pancreatic cholesteryl ester accumulation by affecting exchange of cholesterol between serum and pancreatic tissue.

Alcohol causes a fatty pancreas. A rat model of ethanol-induced pancreatic steatosis.

To develop an animal mode of alcoholic pancreatic steatosis, female Wistar rats were pair fed liquid diets, containing ethanol as 36% of calories or an isocaloric amount of carbohydrate for 3 weeks. Electron microscopic examination showed lipid vesicles localized principally at the bases of pancreatic acinar cells in the ethanol-fed rats. Ethanol feeding significantly increased pancreatic content of cholesteryl ester without changing levels of other lipids. Ethanol feeding enhanced labeled acetate, palmitate, oleate, and linoleate incorporation into cholesteryl ester. Therefore, increased esterification of cholesterol may, in part, explain the observed accumulation of cholesteryl ester.

Inhibition of the chronic ethanol-induced fatty liver by antioxidant administration.

SummaryFemale rats were maintained for 21 days on nutritionally adequate liquid diets containing either “low” or “high” fat content and supplemented with ethanol or isocaloric sucrose as 35% of the calories. Liver triglyceride concentrations were significantly elevated in animals maintained on both diets supplemented with ethanol. However, a greater increment in triglyceride concentrations was manifested in the “high” fat ethanol group under conditions of similar caloric intake. The intraperitoneal administration of the lipid antioxidant, N,N′-diphenyl-p-phenylenediamine (DPPD), prior to, and during the dietary period significantly inhibited the ethanol-induced increment in hepatic triglyceride concentration. The inhibition of the chronic ethanol-induced steatosis, in conjuction with our previous studies of antioxidant modification of the acute ethanol-in-duced hepatic lesion, further accents the possible role of lipid peroxidation as a determinant in cell injury and the role of antioxidants as liver prot...