Influence of dietary content of lipids and lipotropic nutrients on chemical carcinogenesis in rats.

High incidences of breast and colon tumors are associated with high dietary fat intake. The importance of specific fat type and of other nutrients that interact with fat, as well as the mechanisms by which fat acts, is being investigated in animal models. The amount and type of dietary fat influence mammary gland carcinogenesis in rats. Tumor incidence and number are increased and latency is decreased in rats fed large amounts of corn oil, other polyunsaturated vegetable oils, or lard. Certain fats, e.g., rapeseed oil and beef fallow, have little or no effect. The influence of corn oil is exerted during promotion; lard appears to act both at initiation and during promotion. Mechanisms proposed for enhancement of carcinogenesis by dietary fat include alteration of endocrine balance and stimulation of cell division or changes in differentiation in the mammary gland. Data from studies of these postulated mechanisms are inconclusive; further investigation in well-defined animal models is needed. Colon carcinogenesis also is increased in rats fed high-fat diets in certain models, but in others there is no demonstrable effect of dietary fat. Interactions of fat and selenium, the requirement for which is governed by amount and type of dietary fat, may play a role in mammary gland and colon carcinogenesis. Lipotropic nutrients, required for normal fat metabolism, have powerful effects on hepatocarcinogenesis but have not been demonstrated to influence colon and mammary gland carcinogenesis. Lipotrope deficiency alters carcinogen metabolism, increases hepatocyte turnover, and accelerates induction of hyperplastic foci in the liver by many carcinogens. The significance of these abnormalities for carcinogenesis and the timing of the lipotrope effects are subjects of investigation in several animal models.