Caloric restriction (CR), the consumption of fewer calories without malnutrition, and reduced insulin and/or IGFI receptor signaling delay many age-related physiological changes and extend the lifespan of many model organisms. Here, we present and review microarray and biochemical studies indicating that the potent anticancer effects of CR and disrupted insulin/IGFI receptor signaling evolved as a byproduct of the role of many mitotic tissues as reservoirs of metabolic energy. We argue that the longevity effects of CR are derived from repeated cycles of apoptosis and autophagic cell death in mitotically competent tissues and protein turnover and cellular repair in postmitotic tissues. We review studies showing that CR initiated late in life can rapidly induce many of the benefits of lifelong CR, including its anticancer effects. We also discuss evidence from liver and heart indicating that many benefits of lifelong CR are recapitulated in mitotic and postmitotic tissues when CR is initiated late in life.

中文翻译：

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在有丝分裂和有丝分裂后组织中对热量限制和改变的IGFI信号传导的保守和组织特异性遗传和生理反应。

热量限制（CR），消耗较少的卡路里而没有营养不良，胰岛素和/或IGFI受体信号传导减少会延迟许多与年龄相关的生理变化，并延长许多模型生物的寿命。在这里，我们目前和审查微阵列和生化研究表明，CR和中断的胰岛素/ IGFI受体信号的强大抗癌作用演变为许多有丝分裂组织作为代谢能量的作用的副产品。我们认为，CR的长寿效应源自有丝分裂感受态组织中细胞凋亡和自噬细胞死亡的反复循环以及有丝分裂后组织中的蛋白质更新和细胞修复。我们审查了研究，发现CR起源于生命的晚期可以迅速诱导出终身CR的许多益处，包括抗癌作用。