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Insulin and aging.

机译：胰岛素和衰老。

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In invertebrates, signaling pathways homologous to mammalian insulin and insulin-like growth factor (IGF-1) signal transduction have a major role in the control of longevity. There are numerous indications that these pathways also influence aging in mammals, but separating the role of insulin from the effects of IGF-1 and growth hormone (GH) is difficult. In mice, selective disruption of the insulin receptor in the adipose tissue extends longevity. Increases in lifespan were also reported in mice with deletion of insulin receptor substrate 1 (IRS1) in whole body or IRS2 only in the brain. GH deficiency or resistance in mutant mice leads to hypoinsulinemia and enhanced insulin sensitivity along with remarkably extended longevity. These characteristics resemble animals subjected to calorie restriction. Studies of physiological characteristics and polymorphisms of insulin-related genes in exceptionally long-lived people suggest a role of insulin signaling in the control of human aging.
机译：在无脊椎动物中，与哺乳动物胰岛素和胰岛素样生长因子（IGF-1）信号转导同源的信号通路在控制寿命方面起着重要作用。有许多迹象表明，这些途径也影响哺乳动物的衰老，但是很难将胰岛素的作用与IGF-1和生长激素（GH）的作用分开。在小鼠中，脂肪组织中胰岛素受体的选择性破坏延长了寿命。据报道，小鼠体内胰岛素受体底物1（IRS1）缺失或仅脑内IRS2缺失，小鼠的寿命也有所增加。突变小鼠中的GH缺乏症或耐药性会导致低胰岛素血症和胰岛素敏感性增强，以及寿命显着延长。这些特征类似于受到卡路里限制的动物。对寿命长的人群中胰岛素相关基因的生理特征和多态性的研究表明，胰岛素信号传导在控制人类衰老中具有重要作用。

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