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Insulin/IGF-1 paradox of aging: Regulation via AKT/IKK/NF-kappa B signaling

机译：胰岛素/ IGF-1衰老悖论：通过AKT / IKK /NF-κB信号调节

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GH/insulin/IGF-1 signaling is a vital pathway e.g. in the regulation of protein synthesis and glucose metabolism. However, mouse dwarf strains which exhibit reduced CH secretion and subsequently a decline in IGF-1 signaling can live longer than their wild type counterparts. There is striking evidence indicating that the IGF-1/PI-3K/AKT signaling enhances growth of animals during development but later in life can potentiate the aging process. This conserved pleiotropy has been called the insulin/IGF-1 paradox. In Caenorhabditis elegans, the decline in this pathway activates the DAF-16gene, an ortholog of mammalian FoxO genes, which regulate stress resistance and longevity. The mammalian PI-3K/AKT pathway also activates the NF-kappa B signaling that inhibits apoptosis and triggers inflammatory responses. Many longevity genes, e.g. FoxOs and SIRT1, are inhibitors of NF-kappa B signaling. We will discuss the evidence that insulin/IGF-1 signaling can enhance the NF-kappa B signaling and subsequently potentiate the aging process and aggravate age-related degenerative diseases.
机译：GH /胰岛素/ IGF-1信号传导是重要的途径，例如在蛋白质合成和葡萄糖代谢的调节中。但是，表现出CH分泌减少并随后IGF-1信号下降的小鼠矮株比其野生型对应株寿命更长。有惊人的证据表明，IGF-1 / PI-3K / AKT信号传导可在发育过程中增强动物的生长，但生命后期可以增强衰老过程。这种保守的多效性被称为胰岛素/ IGF-1悖论。在秀丽隐杆线虫中，该途径的下降激活了DAF-16基因，它是哺乳动物FoxO基因的直系同源基因，可调节抗逆性和寿命。哺乳动物PI-3K / AKT途径还激活NF-κB信号传导，从而抑制细胞凋亡并触发炎症反应。许多长寿基因，例如FoxO和SIRT1是NF-κB信号传导的抑制剂。我们将讨论胰岛素/ IGF-1信号传导可增强NF-κB信号传导并随后增强衰老过程并加剧与年龄有关的退行性疾病的证据。

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