An experimental paradigm for studying the cellular and molecular mechanisms of cancer inhibition by energy restriction

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Abstract
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.

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