The arcuate nucleus and neuropeptide Y contribute to the antitumorigenic effect of calorie restriction

Aging Cell

Robin K. Minor²  Miguel López¹  Caitlin M. Younts²  Bruce Jones²  Kevin J. Pearson²  Robert Michael Anson²  Carlos Diéguez¹ 

[1]Department of Physiology, School of Medicine, University of Santiago de Compostela-Instituto de Investigación Sanitaria, S. Francisco s/n, Santiago de Compostela (A Coruña) 15782, Spain

[2]Laboratory of Experimental Gerontology, National Institute on Aging, National Institutes of Health, 251 Bayview Boulevard, Suite 100 Room 9C218, Baltimore, MD 21224, USA

关键词: calorie restriction;    hypothalamus;    monosodium glutamate;    neuroendocrine;    neuropeptide Y;    tumorigenesis;   

DOI  :  10.1111/j.1474-9726.2011.00693.x

来源: Wiley

【 摘 要 】

Summary

Calorie restriction (CR) is known to have profound effects on tumor incidence. A typical consequence of CR is hunger, and we hypothesized that the neuroendocrine response to CR might in part mediate CR’s antitumor effects. We tested CR under appetite suppression using two models: neuropeptide Y (NPY) knockout mice and monosodium glutamate-injected mice. While CR was protective in control mice challenged with a two-stage skin carcinogenesis model, papilloma development was neither delayed nor reduced by CR in the monosodium glutamate-treated and NPY knockout mice. Adiponectin levels were also not increased by CR in the appetite-suppressed mice. We propose that some of CR’s beneficial effects cannot be separated from those imposed on appetite, and that NPY neurons in the arcuate nucleus of the hypothalamus are involved in the translation of reduced intake to downstream physiological and functional benefits.

【 授权许可】

Unknown   
No claim to original US government works. Aging Cell © 2011 Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland