Calcium phosphate supplementation results in lower rat fecal bile acid concentrations and a more quiescent colonic cell proliferation pattern than does calcium lactate.
Lupton J.R. | Chen X.Q. | Frolich W.
Although there is general agreement that dietary calcium is protective against colon carcinogenesis, considerable controversy exists on the relative efficacy of the counterion in calcium supplements. We therefore conducted a comparative study in rats of four forms of calcium supplementation (calcium phosphate, casein, lactate, and a 50:50 phosphate-carbonate combination). The relative effects of these supplements on measurements of colon physiology, in vivo pH, fecal fat, individual bile acids, and in vivo cell proliferation were measured in the same animals. In contrast to results when amounts of calcium are varied, there was no effect of form of supplement on total fecal output or output of fecal fat. Calcium phosphate resulted in the most acidified cecal contents. Calcium phosphate and calcium casein resulted in lower fecal concentrations of lithocholate and lower amounts of total fecal bile acids than supplementation with the calcium lactate or combination diets. In addition, rats fed calcium phosphate had lower concentrations of fecal beta-muricholate than rats provided with the calcium combination supplement. In the proximal colon, calcium phosphate resulted in a significantly lower number of cells per crypt column and a lower labeling index than the calcium lactate diet. The position of the highest labeled cell was lower with calcium phosphate supplementation than with supplementation from the calcium combination or the calcium lactate diet. There was a highly significant correlation between the pH of cecal contents and labeling index in the proximal colon (r = 0.98, p = 0.003). The results suggest that calcium phosphate may inhibit colon tumor incidence more effectively than calcium lactate, because the calcium phosphate group had a lower colonic proliferative status than the calcium lactate group. Changes in the proliferative status of colonocytes are known to precede and accompany neoplasia.
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