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Effects of Deoxycholic Acid and Butyrate on Mucosal Prostaglandin E2 Release and Cell Proliferation in the Human Sigmoid Colon
Author(s) -
Bartram HansPeter,
Scheppach Wolfgang,
Englert Stefan,
Dusel Gerda,
Richter Astrid,
Richter Frank,
Kasper Heinrich
Publication year - 1995
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/0148607195019003182
Subject(s) - deoxycholic acid , butyrate , prostaglandin e2 , lubiprostone , sigmoid colon , chemistry , distal colon , prostaglandin e , cell growth , sigmoid function , prostaglandin , medicine , gastroenterology , biochemistry , bile acid , rectum , computer science , fermentation , chronic constipation , machine learning , constipation , artificial neural network
Background: A high‐fat, low‐fiber diet resulting in increased excretion of fecal secondary bile acids is regarded as a major risk factor for colon cancer. Incubation of human colonic biopsies with the secondary bile acid deoxycholic acid (DCA) leads to hyperproliferation with expansion of the proliferative zone, ie, a biomarker of increased cancer risk. Antiproliferative effects on various colon cancer cell lines, however, were reported for butyrate (BUT), a fermentation product of dietary fiber. Methods: In the following in vitro study we incubated biopsies from the normal sigmoid colon of 12 patients (age 55.8 ± 3.6 years) with 5 μM DCA or a combination of 5 μM DCA plus 10 mM BUT (DCA/BUT) and determined epithelial proliferation by bromodeoxyuridine immunohistochemistry. As a possible mediator for the DCA effects on colonic cell proliferation, mucosal prostaglandin E 2 (PGE 2 ) release into the incubation medium was measured by 125 I‐PGE 2 radioimmunoassay. Results: Incubation with DCA alone revealed a significantly higher labeling index for the whole crypt (.17 vs.11, p <.01) and for the upper 40% of the crypt (.05 vs.01, p <.01) compared with DCA/BUT. Mucosal PGE2 release during DCA/BUT incubation showed a trend toward lower values compared with DCA incubation (357.07 vs 434.29 pg/mg per hour; p =.07). Conclusion: The results indicate a normalization of DCA‐induced hyperproliferation of colonic epithelium by butyrate that is not clearly mediated by PGE 2 . Considering that nutrition affects the luminal concentrations of DCA and butyrate, our findings may have implications for colonic carcinogenesis. (Journal of Parenteral and Enteral Nutrition 19: 182–186, 1995)