RIS ID

25522

Publication Details

Le Leu, R. K., Hu, Y., Brown, I. L. & Young, G. P. (2009). Effect of high amylose maize starches on colonic fermentation and apoptotic response to DNA-damage in the colon of rats. Nutrition & Metabolism, 6 (11), 1-28.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background

We investigated in rats the effects of feeding different forms of high amylose maize starches (HAMS) rich in resistant starch (RS) to understand what the implications of RS heterogeneity might be for colonic biology, including innate cellular responses to DNA-damage.

Methods

A range of maize starches were compared: digestible cornstarch (Control), HYLON® VII, Hi-maize® 1043, Hi-maize® 240, Hi-maize® 260 and NOVELOSE® 330. Included in the comparison was Cellulose. End-points after 4 weeks included: pH, short chain fatty acids (SCFA) levels, colonic epithelial cell kinetics and apoptotic response to carcinogen 'azoxymethane' in the colonic epithelium.

Results

The RS diets significantly increased SCFA and reduced pH in caecal content and faeces. Hi-maize 260 resulted in the highest butyrate concentrations. All RS diets prevented the mucosal atrophy as seen in the rats fed the Control diet. Epithelial cell turnover was increased in the Control and Cellulose groups compared to the Hi-maize 260, HYLON VII and NOVELOSE 330 groups (P < 0.01). The apoptotic response to azoxymethane was higher only in the Hi-maize 260 group compared to the Control group (P < 0.01). Butyrate correlated positively with the apoptotic response (P < 0.01).

Conclusion

The consumption of RS elicits a range of beneficial physiological and protective effects associated with the fermentation of RS. Increased production of butyrate seems a likely explanation by which RS enhances the apoptotic response to carcinogen-induced DNA damage which is consistent with the proposed role of this SCFA in promoting a normal cell phenotype and preventing the development of abnormal cell populations.

 

Link to publisher version (DOI)

http://dx.doi.org/10.1186/1743-7075-6-11