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[Cancer Research 63, 1752-1755, April 15, 2003]
© 2003 American Association for Cancer Research

Advances in Brief

Calorie Restriction and Diet Composition Modulate Spontaneous Intestinal Tumorigenesis in ApcMin Mice through Different Mechanisms1

Volker Mai, Lisa H. Colbert, David Berrigan, Susan N. Perkins, Ruth Pfeiffer, Jackie A. Lavigne, Elaine Lanza, Diana C. Haines, Arthur Schatzkin and Stephen D. Hursting2

Cancer Prevention Fellowship Program, Division of Cancer Prevention [V. M., D. B., S. N. P., J. A. L., S. D. H.], Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics [V. M., R. P., A. S.], Laboratory of Biosystems and Cancer, Center for Cancer Research [V. M., L. H. C., D. B., S. N. P., J. A. L., S. D. H.], and Applied Research Branch, Division of Cancer Control and Population Sciences [D. B.], National Cancer Institute, Bethesda, Maryland 20892; Laboratory of Epidemiology, Demography and Biometry, National Institute on Aging, Bethesda, Maryland 20892 [L. H. C.]; Cancer Prevention Studies Branch, Center for Cancer Research, Bethesda, Maryland 20892 [E. L.]; and Pathology/Histotechnology Laboratory, Science Applications International Corporation–Frederick, Frederick, Maryland 21702 [D. C. H.]

We evaluated the effects of diet on intestinal tumorigenesis in male ApcMin mice by comparing AIN-76A diet fed ad libitum (CON); calorie intake restricted by 40% of the CON (CR); diet high in olive oil and supplemented with freeze-dried fruit and vegetable extracts (OFV); and diet high in total fat (HF). Compared with CON, the frequency of intestinal polyps was reduced by 57% by CR (P < 0.001) and by 33% OFV diet (P = 0.04). Both effective interventions reduced total body weight, lean mass, and fat mass and increased daily urinary corticosterone output, but only CR reduced serum insulin-like growth factor I and leptin. We conclude that dietary interventions can partially offset genetic susceptibility to intestinal carcinogenesis.




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