Skip Navigation



Carcinogenesis Advance Access published online on August 5, 2008

Carcinogenesis, doi:10.1093/carcin/bgn173
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
29/11/2169    most recent
bgn173v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Bajka, B.
Right arrow Articles by Topping, D. L
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bajka, B.
Right arrow Articles by Topping, D. L
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Butyrylated Starch Protects Colonocyte DNA Against Dietary Protein-Induced Damage in Rats

Balazs Bajka1,2,3, Julie M Clarke1,2, Lynne Cobiac3 and David L Topping1,2,4

1 Preventative Health National Research Flagship
2 CSIRO Human Nutrition, Adelaide, South Australia
3 Discipline of Physiology, The School of Molecular and Biomedical Sciences, The University of Adelaide, Department of Medicine, Flinders University, Bedford Park, South Australia

4 Corresponding author: Dr DL Topping, CSIRO Human Nutrition, Kintore Avenue, Adelaide, Australia; Postal address: CSIRO Human Nutrition, PO Box 10041, Adelaide BC 5000, South Australia, Australia. Phone: +61 8 8303 8930 Fax: +61 8 8303 8899, Email: david.topping{at}csiro.au

Dietary resistant starch (RS), as a high amylose maize starch (HAMS), prevents dietary protein-induced colonocyte genetic damage in rats, possibly through the short chain fatty acid (SCFA) butyrate produced by large bowel bacterial RS fermentation. Increasing butyrate availability may improve colonic health and dietary butyrylated starch (HAMSB) is an effective method of achieving this goal. In this study rats (n = 8/group) were fed diets containing high levels (25%) of dietary protein as casein with 10% or 20% dietary HAMSB and HAMS. Colonocyte genetic damage was measured by the comet assay and was 2 fold higher in rats fed 25% protein than those fed 15 % protein (P<0.001). Concurrent feeding of 25% protein and either HAMS or HAMSB lowered genetic damage significantly relative to a low RS high protein control diet. The 20% HAMSB diet was twice as effective as 20% HAMS in opposing genetic damage. Large bowel digesta butyrate was significantly increased in rats fed 10% compared with 20% HAMS, and in rats fed 10% compared with 20% HAMSB. The levels were significantly higher in the HAMSB groups relative to the HAMS groups. Hepatic portal venous SCFA were higher in rats fed HAMS and highest in those fed HAMSB. Caecal digesta ammonia was increased by HAMSB and correlated negatively with digesta pH. Ammonia is cytotoxic and lower digesta pH could lower its absorption, possibly contributing to lower genetic damage. Delivery of butyrate to the large bowel by HAMSB could reduce colo-rectal cancer risk by preventing diet-induced colonocyte genetic damage.

Key Words: butyrate • butyrylated starch • colonocyte genotoxicity • rats

Received May 19, 2008; revised July 14, 2008; accepted July 15, 2008.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.