2.50
Hdl Handle:
http://hdl.handle.net/10146/68414
Title:
Does butyrate protect from colorectal cancer?
Authors:
Sengupta, Shomik; Muir, Jane G.; Gibson, Peter R.
Abstract:
Butyrate, the four-carbon fatty acid, is formed in the human colon by bacterial fermentation of carbohydrates (including dietary fiber), and putatively suppresses colorectal cancer (CRC). Butyrate has diverse and apparently paradoxical effects on cellular proliferation, apoptosis and differentiation that may be either pro-neoplastic or anti-neoplastic, depending upon factors such as the level of exposure, availability of other metabolic substrate and the intracellular milieu. In humans, the relationship between luminal butyrate exposure and CRC has been examined only indirectly in case-control studies, by measuring fecal butyrate concentrations, although this may not accurately reflect effective butyrate exposure during carcinogenesis. Perhaps not surprisingly, results of these investigations have been mutually contradictory. The direct effect of butyrate on tumorigenesis has been assessed in a number of in vivo animal models, which have also yielded conflicting results. In part, this may be explained by methodological differences in the amount and route of butyrate administration, which are likely to significantly influence delivery of butyrate to the distal colon. Nonetheless, there appears to be some evidence that delivery of an adequate amount of butyrate to the appropriate site protects against early tumorigenic events. Future study of the relationship between butyrate and CRC in humans needs to focus on risk stratification and the development of feasible strategies for butyrate delivery.
Citation:
J. Gastroenterol. Hepatol. 2006, 21 (1 Pt 2):209-218
Journal:
Journal of gastroenterology and hepatology
Issue Date:
Jan-2006
URI:
http://hdl.handle.net/10146/68414
DOI:
10.1111/j.1440-1746.2006.04213.x
PubMed ID:
16460475
Additional Links:
http://www3.interscience.wiley.com/journal/118622274/abstract?CRETRY=1&SRETRY=0
Type:
Article
Language:
en
Description:
KEYWORDS - CLASSIFICATION: Animals;Anticarcinogenic Agents;Butyrates;Cell Proliferation;Colon;Colorectal Neoplasms;dietary modulation of cancer & cancer biomarkers;drug effects;Dietary Fiber;Evaluation;Humans;mechanisms of carcinogenesis;metabolism;pathology;pharmacology;physiopathology;prevention & control.
ISSN:
0815-9319
Appears in Collections:
Articles with annotation

Full metadata record

DC FieldValue Language
dc.contributor.authorSengupta, Shomik-
dc.contributor.authorMuir, Jane G.-
dc.contributor.authorGibson, Peter R.-
dc.date.accessioned2009-05-18T06:59:58Z-
dc.date.available2009-05-18T06:59:58Z-
dc.date.issued2006-01-
dc.identifier.citationJ. Gastroenterol. Hepatol. 2006, 21 (1 Pt 2):209-218en
dc.identifier.issn0815-9319-
dc.identifier.pmid16460475-
dc.identifier.doi10.1111/j.1440-1746.2006.04213.x-
dc.identifier.urihttp://hdl.handle.net/10146/68414-
dc.descriptionKEYWORDS - CLASSIFICATION: Animals;Anticarcinogenic Agents;Butyrates;Cell Proliferation;Colon;Colorectal Neoplasms;dietary modulation of cancer & cancer biomarkers;drug effects;Dietary Fiber;Evaluation;Humans;mechanisms of carcinogenesis;metabolism;pathology;pharmacology;physiopathology;prevention & control.en
dc.description.abstractButyrate, the four-carbon fatty acid, is formed in the human colon by bacterial fermentation of carbohydrates (including dietary fiber), and putatively suppresses colorectal cancer (CRC). Butyrate has diverse and apparently paradoxical effects on cellular proliferation, apoptosis and differentiation that may be either pro-neoplastic or anti-neoplastic, depending upon factors such as the level of exposure, availability of other metabolic substrate and the intracellular milieu. In humans, the relationship between luminal butyrate exposure and CRC has been examined only indirectly in case-control studies, by measuring fecal butyrate concentrations, although this may not accurately reflect effective butyrate exposure during carcinogenesis. Perhaps not surprisingly, results of these investigations have been mutually contradictory. The direct effect of butyrate on tumorigenesis has been assessed in a number of in vivo animal models, which have also yielded conflicting results. In part, this may be explained by methodological differences in the amount and route of butyrate administration, which are likely to significantly influence delivery of butyrate to the distal colon. Nonetheless, there appears to be some evidence that delivery of an adequate amount of butyrate to the appropriate site protects against early tumorigenic events. Future study of the relationship between butyrate and CRC in humans needs to focus on risk stratification and the development of feasible strategies for butyrate delivery.en
dc.language.isoenen
dc.relation.urlhttp://www3.interscience.wiley.com/journal/118622274/abstract?CRETRY=1&SRETRY=0en
dc.subjectCancer chemopreventionen
dc.subjectColonic fermentationen
dc.subjectDietary fiberen
dc.subjectDietary preventionen
dc.subjectShort-chain fatty acidsen
dc.subject.meshAnimals-
dc.subject.meshAnticarcinogenic Agents-
dc.subject.meshButyrates-
dc.subject.meshCell Proliferation-
dc.subject.meshColon-
dc.subject.meshColorectal Neoplasms-
dc.subject.meshDietary Fiber-
dc.subject.meshHumans-
dc.titleDoes butyrate protect from colorectal cancer?en
dc.typeArticleen
dc.identifier.journalJournal of gastroenterology and hepatologyen

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