Holzenberger Martin
Centre de Recherche Inserm, Bâtiment Kourilsky, Hôpital Saint-Antoine, 75571 Paris Cedex 12, France.
Med Sci (Paris). 2009 Apr;25(4):371-6. doi: 10.1051/medsci/2009254371.
Using a mouse model relevant for humans, lifespan can be prolonged by reducing IGF-I signaling selectively in the central nervous system. This effect occurred through changes in specific neuroendocrine pathways. Investigating the pathophysiological mechanism, we found that IGF receptors in the brain steered the development of the somatotropic axis, which in turn altered the individual growth trajectory and lifespan. Our work is experimental proof that chronically low IGF-I and low growth hormone (GH) levels favor long lifespan and postpone age-related mortality. Our results, together with other recent reports, challenge the notion that GH can slow down or prevent human aging. This is important because growth hormone is sometimes proposed to elderly people as a substitutive treatment in order to compensate the negative effects of aging.
使用与人类相关的小鼠模型，通过选择性地降低中枢神经系统中的IGF-I信号传导，可以延长寿命。这种效应是通过特定神经内分泌途径的变化而发生的。在研究病理生理机制时，我们发现大脑中的IGF受体引导了生长激素轴的发育，进而改变了个体的生长轨迹和寿命。我们的研究是长期低IGF-I和低生长激素（GH）水平有利于长寿并推迟与年龄相关死亡率的实验证据。我们的结果与其他近期报告一起，挑战了生长激素可以减缓或预防人类衰老的观点。这很重要，因为生长激素有时被建议作为老年人的替代疗法，以补偿衰老的负面影响。
