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

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.
AuthorsZongjian Zhu, Weiqin Jiang, Henry J Thompson
JournalMolecular carcinogenesis (Mol Carcinog) Vol. 35 Issue 2 Pg. 51-6 (Oct 2002) ISSN: 0899-1987 [Print] United States
PMID12325034 (Publication Type: Comparative Study, Journal Article, Research Support, U.S. Gov't, P.H.S.)
CopyrightCopyright 2002 Wiley-Liss, Inc.
Chemical References
  • Leptin
  • Receptors, Estrogen
  • Insulin-Like Growth Factor I
  • Methylnitrosourea
  • Corticosterone
Topics
  • Adenocarcinoma (chemically induced, metabolism, prevention & control)
  • Animals
  • Caloric Restriction
  • Corticosterone (blood)
  • Diet
  • Energy Metabolism
  • Female
  • Insulin-Like Growth Factor I (metabolism)
  • Leptin (blood)
  • Mammary Glands, Animal (pathology)
  • Mammary Neoplasms, Experimental (chemically induced, metabolism, prevention & control)
  • Methylnitrosourea
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Estrogen (metabolism)

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