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Author Notes:

Address correspondence to Viviana I Pérez, PhD, Department of Biochemistry and Biophysics, Linus Pauling Institute, Oregon State University, 307 Linus Pauling Science Center, Corvallis, OR 97331.Email: viviana.perez@oregonstate.edu .

We thank Vivian Diaz and the department of Laboratory Animal Resources at University Health Science Center at San Antonio for mice husbandry and Elizabeth Fernandez.

Subjects:

Research Funding:

Financial support was provided by The San Antonio Nathan Shock Aging Center (1P30-AG-13319 to A.R.), National Institut es of Health (NIH) RC2 Grand Opportunity grant (AG036613 to A.R.), NIH T32 Training Grant (AG021890 to W.C.F.), and The Ellison Medical Foundation (to V.I.P.).

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Geriatrics & Gerontology
  • Gerontology
  • GERIATRICS & GERONTOLOGY
  • GERONTOLOGY
  • Rapamycin
  • Dietary restriction
  • mTOR
  • Autophagy
  • Gene expression
  • GLUTATHIONE REDOX STATE
  • GENETICALLY HETEROGENEOUS MICE
  • EXTENDS LIFE-SPAN
  • CELL-CYCLE ARREST
  • CALORIE RESTRICTION
  • OXIDATIVE STRESS
  • RAT HEPATOCYTES
  • MTOR INHIBITION
  • UREA CYCLE
  • LONGEVITY

Short-Term Treatment With Rapamycin and Dietary Restriction Have Overlapping and Distinctive Effects in Young Mice

Journal Title:

Journals of Gerontology, Series A

Volume:

Volume 68, Number 2

Publisher:

, Pages 108-116

Type of Work:

Article | Final Publisher PDF

Abstract:

Because rapamycin, an inhibitor of the nutrient sensor mammalian target of rapamycin, and dietary restriction both increase life span of mice, it has been hypothesized that they act through similar mechanisms. To test this hypothesis, we compared various biological parameters in dietary restriction mice (40% food restriction) and mice fed rapamycin (14 ppm). Both treatments led to a significant reduction in mammalian target of rapamycin signaling and a corresponding increase in autophagy. However, we observed striking differences in fat mass, insulin sensitivity, and expression of cell cycle and sirtuin genes in mice fed rapamycin compared with dietary restriction. Thus, although both treatments lead to significant downregulation of mammalian target of rapamycin signaling, these two manipulations have quite different effects on other physiological functions suggesting that they might increase life span through a common pathway as well as pathways that are altered differently by dietary restriction and rapamycin.

Copyright information:

© 2012 The Author. Published by Oxford University Press on behalf of The Gerontological Society of America. Attribution-NonCommercial 2.0 UK: England & Wales (CC BY-NC 2.0 UK)

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial 2.0 Generic License (http://creativecommons.org/licenses/by-nc/2.0/).

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