The correlation between cholecystectomy and fecal bile acids, and large-bowel cancer induced with 1,2-dimethylhydrazine in mice.
The relationship between cholecystectomy and large-bowel cancer development was investigated in animal models. Female ICR mice underwent cholecystectomy, and received 15 weekly intragastric administrations (Experiment 1) or 10 weekly subcutaneous injections (Experiment 2) of 15 mg/kg body weight of large-bowel carcinogen 1,2-dimethylhydrazine (DMH). Autopsy at 28 weeks after surgery showed that cholecystectomized mice had a nonsignificantly increased incidence of large-bowel carcinomas, compared to sham-operated and/or unoperated control mice (85 vs. 64 percent in Experiment 1; 31 vs. 16 and 20 percent in Experiment 2). Cholecystectomy alone without DMH treatment did not produce any cancer. Cholecystectomized mice excreted a significantly increased level of primary bile acids but an unchanged level of secondary bile acids in the feces, compared with unoperated control mice. It is obvious that cholecystectomy enhanced the development of DMH-induced, large-bowel carcinomas along with the change of fecal bile acid composition, suggesting that changes of bile acid metabolism after cholecystectomy may enhance or promote large-bowel carcinogenesis in man as well. This association of cholecystectomy and large-bowel cancer is not a strong one, however, as presented in epidemiologic as well as experimental studies.
D000818:Animals; D001647:Bile Acids and Salts / Q000378:metabolism*; D002763:Cholecystectomy / Q000009:adverse effects*; D003043:Cocarcinogenesis; D004127:Dimethylhydrazines; D005243:Feces / Q000378:metabolism*; D005260:Female; D007414:Intestinal Neoplasms / Q000139:chemically induced / Q000209:etiology* / Q000378:metabolism; D007420:Intestine, Large / Q000378:metabolism; D051379:Mice; D008815:Mice, Inbred Strains
D001647:Bile Acids and Salts; D004127:Dimethylhydrazines