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Tracking changes in hypothalamic igf-1 sensitivity with aging and caloric restriction

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Tracking changes in hypothalamic IGF-1 sensitivity with aging and caloric restriction.

F. Yaghmaie [1], O. Saeed [2], S.A. Garan [3], A.M. Gouw [4], P. Jafar [4], J. Kaur [4], S. Nijjar [4], P.S. Timiras [4], H. Sternberg [5], M.A. Voelker [5]. [1] Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA, [2] New York Medical College, Valhalla, New York, USA, [3] Aging Research Centre, Waterloo, Ontario, Canada, [4] Department of Molecular and Cell Biology, University of California, Berkeley, USA, [5] BioTime, Inc., Berkeley, California, USA

Manipulating IGF-1 signaling in the neuroendocrine system reliably extends the mammalian lifespan, yet the basic descriptive biology concerning IGF-1 Receptor (IGF-1R) density and distribution throughout the lifespan is lacking. By tracking changes in hypothalamic IGF-1 sensitivity with both normal aging and life-long caloric restriction, the IGF-1R biomarkers of aging can be determined while simultaneously evaluating the role of IGF-1 signaling in CR’s life extending effect. Of the hypothalamic nuclei that express IGF-1 Receptor (IGF-1R), the cells of the Supraoptic nucleus (SON) and Paraventricular nucleus (PVN) display the most robust IGF-1R expression. Taking IGF-1R immunoreactivity as an index of sensitivity to IGF-1, this investigation counted IGF-1R-immunoreactive and non-immunoreactive cells in the SON and PVN of young-ad-libitum fed (young-Al, 6 weeks), old ad-libitum fed (Old-Al, 22 months), and old calorie restricted (Old-CR, 22 months) female B6D2F1 mice. An automated imaging microscopy system (AIMS) was used to generate cell counts for each section of hypothalamus. Results show that both SON and PVN lose about one-third of IGF-1R immunoreactive cells with normal aging. Also, Old-CR mice lost higher numbers of IGF-1R non-immunoreactive cells while maintaining similar counts of IGF-1R immunoreactive cells in comparison to Old-Al mice. Consequently, Old-CR mice show a higher percentage of IGF-1R immunoreactive cells reflecting increased hypothalamic sensitivity to IGF-1 in comparison to normally aging mice. Supported by NIH AG19145-05 and BioTime, Inc.

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