Resistant starch prevents colonic DNA damage induced by high dietary cooked red meat or casein in rats

被引:94
作者
Toden, Shusuke
Bird, Anthony R.
Topping, David L.
Conlon, Michael A.
机构
[1] CSIRO Human Nutr, Adelaide, SA 5000, Australia
[2] CSIRO Food Futures Natl Res, Flagship, Australia
[3] Univ Adelaide, Sch Mol Sci, Discipline Physiol, Adelaide, SA, Australia
关键词
resistant starch; red meat; casein; colon; genotoxicity;
D O I
10.4161/cbt.5.3.2382
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
In a previous study we have shown that high levels of dietary protein ( as casein) result in increased levels of colonic DNA damage, measured by the comet assay, and thinning of the colonic mucus layer in rats when dietary resistant starch (RS) is negligible. Feeding RS abolishes these effects. This study aimed to establish whether a diet high in protein as cooked red meat would have similar effects and whether RS was protective. Rats were fed a diet containing 15% or 25% casein or 25% cooked lean red beef, each with or without the addition of 48% high amylose maize starch ( a rich source of RS) for four weeks. As expected, high dietary casein caused a 2-fold increase in colonic DNA damage compared with a low casein diet and reduced the thickness of the colonic mucus layer by 41%. High levels of cooked meat caused 26% greater DNA damage than the high casein diet but reduced mucus thickness to a similar degree to casein. Addition of RS to the diet abolished the increase in DNA damage and the loss of colonic mucus thickness induced by either high protein diet. Cecal and fecal short chain fatty acid pools were also increased by inclusion of RS in the diet. Because DNA damage is an early step in the initiation of cancer, these findings suggest that increased DNA damage due to high dietary protein as cooked red meat or casein could increase colorectal cancer risk but inclusion of resistant starch in the diet could significantly reduce that risk.
引用
收藏
页码:267 / 272
页数:6
相关论文
共 52 条
[1]  
Anderson D, 1999, TERATOGEN CARCIN MUT, V19, P137, DOI 10.1002/(SICI)1520-6866(1999)19:2<137::AID-TCM6>3.0.CO
[2]  
2-2
[3]   Repression of MUC2 gene expression by butyrate, a physiological regulator of intestinal cell maturation [J].
Augenlicht, L ;
Shi, L ;
Mariadason, J ;
Laboisse, C ;
Velcich, A .
ONCOGENE, 2003, 22 (32) :4983-4992
[4]   Does increased endogenous formation of N-nitroso compounds in the human colon explain the association between red meat and colon cancer? [J].
Bingham, SA ;
Pignatelli, B ;
Pollock, JRA ;
Ellul, A ;
Malaveille, C ;
Gross, G ;
Runswick, S ;
Cummings, JH ;
ONeill, IK .
CARCINOGENESIS, 1996, 17 (03) :515-523
[5]   Resistant starch lowers fecal concentrations of ammonia and phenols in humans [J].
Birkett, A ;
Muir, J ;
Phillips, J ;
Jones, G ;
ODea, K .
AMERICAN JOURNAL OF CLINICAL NUTRITION, 1996, 63 (05) :766-772
[6]   PRODUCTION OF URINARY PHENOLS BY GUT BACTERIA AND THEIR POSSIBLE ROLE IN CAUSATION OF LARGE BOWEL CANCER [J].
BONE, E ;
TAMM, A ;
HILL, M .
AMERICAN JOURNAL OF CLINICAL NUTRITION, 1976, 29 (12) :1448-1454
[7]   Resistant starch and "the butyrate revolution" [J].
Brouns, F ;
Kettlitz, B ;
Arrigoni, E .
TRENDS IN FOOD SCIENCE & TECHNOLOGY, 2002, 13 (08) :251-261
[8]   Colonic mucus: secretion and turnover in relation to dietary fibre intake [J].
Brownlee, IA ;
Havler, ME ;
Dettmar, PW ;
Adrian, A ;
Pearson, JP .
PROCEEDINGS OF THE NUTRITION SOCIETY, 2003, 62 (01) :245-249
[9]  
BRYAN GT, 1971, AM J CLIN NUTR, V24, P841
[10]  
Caderni G, 2003, CANCER RES, V63, P2388