Aging
Navigate
Submit an Article
Research Paper|Volume 8, Issue 3|pp 539—546

Measuring aging rates of mice subjected to caloric restriction and genetic disruption of growth hormone signaling

Jacob J.E. Koopman1,2, Diana van Heemst1,2, David van Bodegom1,2, Michael S. Bonkowski3,4, Liou Y. Sun3,5, Andrzej Bartke3
  • 1Section of Gerontology and Geriatrics, Department of Internal Medicine, Leiden University Medical Center, Leiden, the Netherlands
  • 2Leyden Academy on Vitality and Ageing, Leiden, the Netherlands
  • 3Division of Geriatric Research, Department of Internal Medicine, Southern Illinois University School of Medicine, Springfield, IL 62794-9628, USA
  • 4Paul F. Glenn Laboratory, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
  • 5Department of Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
Received: January 12, 2016Accepted: February 3, 2016Published: March 7, 2016
https://doi.org/10.18632/aging.100919

Copyright: © 2016 Koopman et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Caloric restriction and genetic disruption of growth hormone signaling have been shown to counteract aging in mice. The effects of these interventions on aging are examined through age-dependent survival or through the increase in age-dependent mortality rates on a logarithmic scale fitted to the Gompertz model. However, these methods have limitations that impede a fully comprehensive disclosure of these effects. Here we examine the effects of these interventions on murine aging through the increase in age-dependent mortality rates on a linear scale without fitting them to a model like the Gompertz model. Whereas these interventions negligibly and non-consistently affected the aging rates when examined through the age-dependent mortality rates on a logarithmic scale, they caused the aging rates to increase at higher ages and to higher levels when examined through the age-dependent mortality rates on a linear scale. These results add to the debate whether these interventions postpone or slow aging and to the understanding of the mechanisms by which they affect aging. Since different methods yield different results, it is worthwhile to compare their results in future research to obtain further insights into the effects of dietary, genetic, and other interventions on the aging of mice and other species.