THE INFLUENCE OF PRENATAL AND POSTNATAL CALORIC-INTAKE ON COLON CARCINOGENESIS

被引:13
作者
NEWBERNE, PM
BUECHE, D
SUPHIPHAT, V
SCHRAGER, TF
SAHAPHONG, S
机构
[1] Department of Pathology, Mallory Institute of Pathology, University School of Medicine, Boston
来源
NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL | 1990年 / 13卷 / 03期
关键词
D O I
10.1080/01635589009514057
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Mother rats were allowed to litter under conventional conditions. They were fed a complete, semipurified diet during gestation, and at time of littering the numbers of pups were reduced to either eight per litter or four per litter in two additional groups. At weaning, all rats were continued on the same diet that their mothers had consumed. One group of those reduced to four per litter at birth was allowed to continue to eat ad libitum while the other group, reduced to four per litter, was pair fed to the ad libitum eight per litter group. The group reduced to four per litter at birth and allowed to eat ad libitum during postnatal life gained the most weight and were heaviest at the termination of the study. This group also had the greater incidence and frequency of colon tumors when exposed to dimethylhydrazine (DMH). The group pair fed to rats fed conventional diets, eight rats per litter, had an incidence and frequency of tumors between the other two groups. These data demonstrate that early exposure to excess calories increased risk for cancer and that early and late excess caloric intake further increased risk. Thus, pre- and perinatal caloric intake may have a significant influence on susceptability to cancer later in life. Mechanisms are only speculative but may include differences in metabolism and modulation of hormonal balance. © 1990, Taylor & Francis Group, LLC. All rights reserved.
引用
收藏
页码:165 / 173
页数:9
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  • [1] American Cancer Society, Cancer Facts and Figures, (1988)
  • [2] Doll R., Peto R., The Cause of Cancer With Quantitative Estimates of Avoidable Risks of Cancer in the United States Today, JNCI, 66, pp. 1191-1308, (1981)
  • [3] Nauss K.M., Jacobs L.R., Newberne P.M., Dietary Fat and Fiber: Relationship to Caloric Intake, Body Growth, and Colon Tumorigenesis, Am J Clin Nutr, 45, pp. 243-251, (1987)
  • [4] Reddy B.S., Amount and Type of Dietary Fat and Colon Cancer in Animal Model Studies, Dietary Fat and Cancer, pp. 295-310, (1986)
  • [5] Newberne P.M., Schrager T.F., Conner M.W., Experimental Evidence on the Nutritional Prevention of Cancer, Nutrition and Cancer Prevention: Investigating the Role of Micronutrients, pp. 33-82, (1989)
  • [6] Rogers A.E., Nauss K.M., Contributions of Laboratory Animal Studies to Colon Carcinogenesis, Large Bowel Cancer: Clinical and Basic Science Research, pp. 1-45, (1985)
  • [7] Newberne P.M., Nauss K.M., Dietary Fat and Colon Cancer: Variable Results in Animal Models, Dietary Fat and Cancer, pp. 311-330, (1986)
  • [8] Madigan S., Laurance V., Stat Plus: A General Statistics Package for the Apple II. Northridge, (1982)
  • [9] Dixon W.J., Brown M.B., BMDP-79: Biomedical Computer Programs P-Series, (1979)
  • [10] McCay C.M.A., Dietary and Aging, Vitamins and Hormones, pp. 147-170, (1949)