An experimental paradigm for studying the cellular and molecular mechanisms of cancer inhibition by energy restriction
✍ Scribed by Zongjian Zhu; Weiqin Jiang; Henry J. Thompson
- Publisher
- John Wiley and Sons
- Year
- 2002
- Tongue
- English
- Weight
- 88 KB
- Volume
- 35
- Category
- Article
- ISSN
- 0899-1987
- DOI
- 10.1002/mc.10073
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✦ Synopsis
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. © 2002 Wiley‐Liss, Inc.