An experimental paradigm for studying the cellular and molecular mechanisms of cancer inhibition by energy restriction.
With a rapid-emergence, chemically induced animal model for breast cancer, an experiment designed to test the hypothesis that energy restriction (ER) induces the loss of carcinogen-initiated cells from the mammary gland, thereby conferring a permanent protective effect against the development of cancer, failed to support this hypothesis. Nonetheless, this experiment served to define an experimental approach and a time frame on which to focus mechanistic inquiry. With an ER and energy repletion (ER-REP) protocol as a tool for identifying potential mediators of the cancer-inhibitory activity of ER, concomitant changes in plasma corticosterone and insulin-like growth factor 1 during energy restriction and repletion were observed. The relationship of the timing of these hormonal changes to the time frame of change in the carcinogenic response during ER-REP was consistent with the role of both hormones in mediating the protective effects of ER. However, a similar pattern of change in the energy-regulated hormone leptin indicated that its role in cancer inhibition also merits consideration.
D000230:Adenocarcinoma / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D000818:Animals; D031204:Caloric Restriction; D003345:Corticosterone / Q000097:blood; D004032:Diet; D004734:Energy Metabolism; D005260:Female; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D020738:Leptin / Q000097:blood; D008321:Mammary Glands, Animal / Q000473:pathology; D008325:Mammary Neoplasms, Experimental / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D008770:Methylnitrosourea; D051381:Rats; D017207:Rats, Sprague-Dawley; D011960:Receptors, Estrogen / Q000378:metabolism
D020738:Leptin; D011960:Receptors, Estrogen; D007334:Insulin-Like Growth Factor I; D008770:Methylnitrosourea; D003345:Corticosterone