Wheat bran diet reduces tumor incidence in a rat model of colon cancer independent of effects on distal luminal butyrate concentrations.
To investigate the effects of dietary fibers in colonic luminal physiology and their role in the prevention of colon cancer, a study was conducted using two diet groups and two treatment groups in a 2 x 2 factorial design. The two diets differed only in the type of dietary fiber, wheat bran and oat bran, and the two treatments were injection with the colon-specific carcinogen azoxymethane, or saline, as a control. There were 34 rats in the carcinogen-injected groups and 11 saline-injected rats per diet group. The goal of the study was to determine if a moderate consumption (6 g/100 g diet) of wheat bran or oat bran would alter the development of colonic tumors in this rat model of colon cancer, and if the differences in tumor incidence were correlated to luminal butyrate concentrations, luminal pH or fecal bulk. Short-chain fatty acid concentrations (SCFA) were measured in feces during the first half of the study (the promotion phase of tumor development) and again at the end of the study. Rats consuming oat bran had greater body weights (P < 0. 002), produced much larger concentrations of all SCFA, including butyrate, in both the proximal and distal colon (P < 0.0001), had more acidic luminal pH values (P < 0.0001), but also had significantly more development of colon tumors (P < 0.03). Alternatively, rats consuming wheat bran produced more typical molar ratios of the SCFA (65:10:20), had a relatively greater concentration of butyrate than propionate, and produced a larger volume (P < 0.05) and more bulky stool than the rats fed oat bran. The results of this study support other evidence that an acidic luminal pH is not protective in and of itself, and that diets containing wheat bran are protective against colon cancer development. In addition, these data show that large luminal butyrate concentrations in the distal colon alone, as were present in the rats consuming oat bran diets, are not protective of tumor development.
Zoran
D L
DL
Faculty of Nutrition, Texas A&M University, College Station, TX 77843-2471, USA.
Turner
N D
ND
Taddeo
S S
SS
Chapkin
R S
RS
Lupton
J R
JR
D000818:Animals; D018554:Avena / Q000592:standards; D001397:Azoxymethane / Q000494:pharmacology; D001835:Body Weight / Q000502:physiology; D002087:Butyrates / Q000032:analysis* / Q000378:metabolism; D002273:Carcinogens / Q000494:pharmacology; D003106:Colon / Q000737:chemistry* / Q000378:metabolism / Q000503:physiopathology; D003110:Colonic Neoplasms / Q000453:epidemiology / Q000378:metabolism / Q000517:prevention & control*; D004032:Diet / Q000592:standards; D004043:Dietary Fiber / Q000494:pharmacology* / Q000627:therapeutic use; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004435:Eating / Q000502:physiology; D005232:Fatty Acids, Volatile / Q000032:analysis / Q000378:metabolism; D005243:Feces / Q000737:chemistry; D006863:Hydrogen-Ion Concentration; D015994:Incidence; D008297:Male; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D014908:Triticum / Q000592:standards*; D015430:Weight Gain / Q000502:physiology
D002087:Butyrates; D002273:Carcinogens; D004043:Dietary Fiber; D005232:Fatty Acids, Volatile; D001397:Azoxymethane