Calcium inhibits the damaging and compensatory proliferative effects of fatty acids on mouse colon epithelium.
Intrarectal instillations of the fatty acids (FA), lauric, linoleic or oleic acids induce inflammation and superficial lysis of the colon epithelium. This reaction is followed by increases in colonic mitotic activity and the number of cells engaged in DNA synthesis in compensatory regeneration for the cells that were lost. This explains, in part, the promotional effect of dietary fat in carcinogenesis. Concomitant oral administration of calcium salts, as CaCO3, largely reduced the mitogenic effects of fatty acids on colon epithelium, presumably by forming biologically inert calcium soaps. Calcium soap formation of dietary fatty acids may be one natural mechanism by which colon epithelium cells are protected hence reducing the impact of dietary fat on carcinogenesis for this organ.
D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D002119:Calcium Carbonate / Q000494:pharmacology; D003106:Colon / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D004247:DNA / Q000096:biosynthesis; D004848:Epithelium / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D005227:Fatty Acids / Q000037:antagonists & inhibitors* / Q000633:toxicity; D005260:Female; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D008938:Mitosis / Q000187:drug effects
D005227:Fatty Acids; D004247:DNA; D002119:Calcium Carbonate; D002118:Calcium