Mechanisms of the intestinal effects of dietary fats and milk products on colon carcinogenesis

Dietary fat may promote colon cancer by increasing fatty acids (FA) and secondary bile acids (BA) in the colonic lumen. These cytotoxic surfactants can damage colonic epithelial cells and thus induce a compensatory hyperproliferation of crypt cells. Our studies show that the hyperproliferative effec...

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Bibliographic Details
Published in:Cancer letters 1997-03, Vol.114 (1), p.75-83
Main Authors: Van der Meer, R., Lapré, J.A., Govers, M.J.A.P., Kleibeuker, J.H.
Format: Article
Language:English
Subjects:
Animal fat
Animals
Bile acids
Bile Acids and Salts - chemistry
Bile Acids and Salts - physiology
Biological and medical sciences
Calcium - pharmacology
Carcinogenesis, carcinogens and anticarcinogens
Cell Division - drug effects
Chemical agents
Colon cancer
Colonic Neoplasms - etiology
Cytotoxicity
Dietary calcium
Dietary Fats - metabolism
Epithelium - drug effects
Fatty Acids - chemistry
Humans
Hyperproliferation
Intestinal Mucosa - drug effects
Intestinal Mucosa - metabolism
Male
Medical sciences
Milk - metabolism
Phosphates - pharmacology
Rats
Tumors
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Summary:Dietary fat may promote colon cancer by increasing fatty acids (FA) and secondary bile acids (BA) in the colonic lumen. These cytotoxic surfactants can damage colonic epithelial cells and thus induce a compensatory hyperproliferation of crypt cells. Our studies show that the hyperproliferative effect of type and amount of dietary fat is not simply due to changes in colonic FA and BA. This indicates that an additional, at present unknown, cytotoxic factor is involved. The hyperproliferative effect of dietary fat is inversely related to the amount of calcium in the diet. In rat and man, dietary calcium precipitates colonic cytotoxic surfactants and thus inhibits luminal cytotoxicity. These inhibitory effects on metabolic risk factors suggest a preventive effect of dietary calcium on colon carcinogenesis.
ISSN:0304-3835
1872-7980
DOI:10.1016/S0304-3835(97)04629-6