Koopman Jacob J E, van Heemst Diana, van Bodegom David, Bonkowski Michael S, Sun Liou Y, Bartke Andrzej
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.
Aging (Albany NY). 2016 Mar;8(3):539-46. doi: 10.18632/aging.100919.
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.
热量限制和生长激素信号通路的基因破坏已被证明可对抗小鼠衰老。这些干预措施对衰老的影响是通过年龄依赖性存活率或通过拟合Gompertz模型的对数尺度上年龄依赖性死亡率的增加来检验的。然而，这些方法存在局限性，阻碍了对这些影响的全面揭示。在这里，我们通过线性尺度上年龄依赖性死亡率的增加来检验这些干预措施对小鼠衰老的影响，而不将它们拟合到像Gompertz模型这样的模型中。当通过对数尺度上的年龄依赖性死亡率进行检验时，这些干预措施对衰老率的影响微不足道且不一致，但当通过线性尺度上的年龄依赖性死亡率进行检验时，它们会导致衰老率在较高年龄时增加到更高水平。这些结果增加了关于这些干预措施是延缓还是减缓衰老的争论，并增进了对它们影响衰老机制的理解。由于不同的方法产生不同的结果，因此在未来的研究中比较它们的结果是值得的，以便进一步深入了解饮食、基因和其他干预措施对小鼠和其他物种衰老的影响。
