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Carcinogenicity of deoxycholate, a secondary bile acid

High dietary fat causes increased bile acid secretion into the gastrointestinal tract and is associated with colon cancer. Since the bile acid deoxycholic acid (DOC) is suggested to be important in colon cancer etiology, this study investigated whether DOC, at a high physiologic level, could be a co...

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Autores principales: Bernstein, Carol, Holubec, Hana, Bhattacharyya, Achyut K., Nguyen, Huy, Payne, Claire M., Zaitlin, Beryl, Bernstein, Harris
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer-Verlag 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3149672/
https://www.ncbi.nlm.nih.gov/pubmed/21267546
http://dx.doi.org/10.1007/s00204-011-0648-7
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author Bernstein, Carol
Holubec, Hana
Bhattacharyya, Achyut K.
Nguyen, Huy
Payne, Claire M.
Zaitlin, Beryl
Bernstein, Harris
author_facet Bernstein, Carol
Holubec, Hana
Bhattacharyya, Achyut K.
Nguyen, Huy
Payne, Claire M.
Zaitlin, Beryl
Bernstein, Harris
author_sort Bernstein, Carol
collection PubMed
description High dietary fat causes increased bile acid secretion into the gastrointestinal tract and is associated with colon cancer. Since the bile acid deoxycholic acid (DOC) is suggested to be important in colon cancer etiology, this study investigated whether DOC, at a high physiologic level, could be a colon carcinogen. Addition of 0.2% DOC for 8–10 months to the diet of 18 wild-type mice induced colonic tumors in 17 mice, including 10 with cancers. Addition of the antioxidant chlorogenic acid at 0.007% to the DOC-supplemented diet significantly reduced tumor formation. These results indicate that a high fat diet in humans, associated with increased risk of colon cancer, may have its carcinogenic potential mediated through the action of bile acids, and that some dietary anti-oxidants may ameliorate this carcinogenicity.
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spelling pubmed-31496722011-09-08 Carcinogenicity of deoxycholate, a secondary bile acid Bernstein, Carol Holubec, Hana Bhattacharyya, Achyut K. Nguyen, Huy Payne, Claire M. Zaitlin, Beryl Bernstein, Harris Arch Toxicol Review Article High dietary fat causes increased bile acid secretion into the gastrointestinal tract and is associated with colon cancer. Since the bile acid deoxycholic acid (DOC) is suggested to be important in colon cancer etiology, this study investigated whether DOC, at a high physiologic level, could be a colon carcinogen. Addition of 0.2% DOC for 8–10 months to the diet of 18 wild-type mice induced colonic tumors in 17 mice, including 10 with cancers. Addition of the antioxidant chlorogenic acid at 0.007% to the DOC-supplemented diet significantly reduced tumor formation. These results indicate that a high fat diet in humans, associated with increased risk of colon cancer, may have its carcinogenic potential mediated through the action of bile acids, and that some dietary anti-oxidants may ameliorate this carcinogenicity. Springer-Verlag 2011-01-26 2011 /pmc/articles/PMC3149672/ /pubmed/21267546 http://dx.doi.org/10.1007/s00204-011-0648-7 Text en © The Author(s) 2011 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
spellingShingle Review Article
Bernstein, Carol
Holubec, Hana
Bhattacharyya, Achyut K.
Nguyen, Huy
Payne, Claire M.
Zaitlin, Beryl
Bernstein, Harris
Carcinogenicity of deoxycholate, a secondary bile acid
title Carcinogenicity of deoxycholate, a secondary bile acid
title_full Carcinogenicity of deoxycholate, a secondary bile acid
title_fullStr Carcinogenicity of deoxycholate, a secondary bile acid
title_full_unstemmed Carcinogenicity of deoxycholate, a secondary bile acid
title_short Carcinogenicity of deoxycholate, a secondary bile acid
title_sort carcinogenicity of deoxycholate, a secondary bile acid
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3149672/
https://www.ncbi.nlm.nih.gov/pubmed/21267546
http://dx.doi.org/10.1007/s00204-011-0648-7
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