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Journal of Nutrition Vol. 119 No. 2 February 1989, pp. 235-241
Copyright © 1989 by American Society for Nutrition
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Independent Effects of Fiber and Protein on Colonic Luminal Ammonia Concentration1

Joanne R. Lupton and Linda J. Marchant2

Department of Animal Science/Nutrition, Texas A&M University and Texas Agricultural Experiment Station, College Station, TX 77843

The potential interactive effects of protein and fiber on cecal and colonic surface areas, colonic luminal ammonia concentrations, luminal pH and blood indices of nitrogen metabolism were tested using two levels of protein (8% and 24%) and two types of fiber (8% pectin or cellulose). Pectin supplementation resulted in larger cecal surface areas and longer large intestines than those of rats fed fiber-free or cellulose-supplemented diets. All high protein diets resulted in total large bowel luminal ammonia (NH3 + NH4+) concentrations that were twice as high as their low protein counterparts (P < 0.05). The effect of fiber on ammonia concentration depended on the fiber type. In the distal colon, pectin-fed animals had three times the ammonia concentration of the fiber-free animals, and 4–5 times the ammonia concentration of the cellulose-fed animals (P < 0.001). Blood urea nitrogen values were higher in the high protein than in the low protein groups (P < 0.05), and highest in the high protein/pectin animals (P < 0.01). This study clearly demonstrates that luminal ammonia concentration is dependent upon both protein level and fiber type, and that a fermentable fiber (pectin), rather than decreasing colonic ammonia concentrations, actually increases them several-fold.


KEY WORDS: • dietary fiber • ammonia • pectin • cellulose • cecal surface area

1 This research was supported by a grant from the Organized Research Fund, Texas A&M University and by Texas Agricultural Experiment Station Project No. 6606. It was presented in part at the Annual Meeting of the Federation of American Societies for Experimental Biology, Washington, D.C., 1987, and has appeared in abstract form (1).

2 Present address: Rhode Island Hospital, Providence, RI 02901.

Manuscript received 6 April 1988. Revision accepted 13 September 1988.




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