| Autor: |
Koopman JJ; Section of Gerontology and Geriatrics, Department of Internal Medicine, Leiden University Medical Center, Leiden, the Netherlands.; Leyden Academy on Vitality and Ageing, Leiden, the Netherlands., van Heemst D; Section of Gerontology and Geriatrics, Department of Internal Medicine, Leiden University Medical Center, Leiden, the Netherlands.; Leyden Academy on Vitality and Ageing, Leiden, the Netherlands., van Bodegom D; Section of Gerontology and Geriatrics, Department of Internal Medicine, Leiden University Medical Center, Leiden, the Netherlands.; Leyden Academy on Vitality and Ageing, Leiden, the Netherlands., Bonkowski MS; Division of Geriatric Research, Department of Internal Medicine, Southern Illinois University School of Medicine, Springfield, IL 62794-9628, USA.; Paul F. Glenn Laboratory, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA., Sun LY; Division of Geriatric Research, Department of Internal Medicine, Southern Illinois University School of Medicine, Springfield, IL 62794-9628, USA.; Department of Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA., Bartke A; Division of Geriatric Research, Department of Internal Medicine, Southern Illinois University School of Medicine, Springfield, IL 62794-9628, USA. |
| Abstrakt: |
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. |
