Carcinogenesis Advance Access first published online on April 5, 2006
This version published online on April 20, 2006
Carcinogenesis, doi:10.1093/carcin/bgl025
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1 Research Group Food Chemistry and Preventive Nutrition, German Institute of Human Nutrition Potsdam-Rehbrücke, D-14558 Nuthetal, Germany; Department of Nutritional Toxicology, German Institute of Human Nutrition Potsdam-Rehbrücke, D-14558 Nuthetal, Germany
* To whom correspondence should be addressed. Some epidemiological and experimental studies suggest that consumption of resistant starch is preventive against colon cancer. Resistant starch leads to a fermentation-mediated increase in the formation of short-chain fatty acids, with a particularly high butyrate fraction in large bowel. Butyrate is considered to be protective against colon cancer because it causes growth arrest and apoptosis and regulates expression of proteins involved in cellular dedifferentiation in various tumor cell lines in culture. We sought to investigate these processes under conditions of a carcinogenicity experiment in vivo. In the present study, 1,2-dimethylhydrazine-treated Sprague-Dawley rats were fed standard diet (n = 12) or diet with 10% hydrothermally modified Novelose 330®, a resistant starch type 3 (RS3), replacing digestible starch (n = 8). After 20 weeks tumor number, epithelial proliferation, apoptosis, immunoreactivity of carcinogenesis-related proteins [protein kinase C-
Received October 13, 2005
Revised February 27, 2006
Accepted March 22, 2006
MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION
Dietary resistant starch type 3 prevents tumor induction by 1,2-dimethylhydrazine and alters proliferation, apoptosis and dedifferentiation in rat colon
Morana Bauer-Marinovic 1 #,
Simone Florian 1 * #,
Katrin Müller-Schmehl 2,
Hansruedi Glatt 3,
and
Gisela Jacobasch 2
2 Research Group Food Chemistry and Preventive Nutrition, German Institute of Human Nutrition Potsdam-Rehbrücke, D-14558 Nuthetal, Germany
3 Department of Nutritional Toxicology, German Institute of Human Nutrition Potsdam-Rehbrücke, D-14558 Nuthetal, Germany
Simone Florian, E-mail: florian{at}mail.dife.de
Abstract 
(PKC-), heat shock protein 25 (HSP25) and gastrointestinal glutathione peroxidase (GI-GPx)], as well as mucin properties were evaluated in proximal and distal colon in situ. No tumors developed under RS3 diet, compared to a tumor incidence of 0.6 ± 0.6 (P < 0.05) under the standard diet. RS3 decreased the number of proliferating cells, the length of the proliferation zone and the total length of the crypt in the distal colon, but not proximal colon, and enhanced apoptosis in both colonic segments. It induced PKC- and HSP25 expression, but inhibited GI-GPx expression in the epithelium of distal colon. RS3 increased the number of predominantly acidic mucin containing goblet cells in the distal colon, but had no effect on the goblet cell count. We conclude that hydrothermally treated RS3 prevented colon carcinogenesis, and that this effect was mediated by enhanced apoptosis of damaged cells accompanied by changes in parameters of dedifferentiation in colonic mucosa.
# These authors contributed equally to this work.
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