Bartke A, Coschigano K, Kopchick J, Chandrashekar V, Mattison J, Kinney B, Hauck S
Department of Physiology, Southern Illinois University School of Medicine, Carbondale, IL 62901-6512, USA.
J Gerontol A Biol Sci Med Sci. 2001 Aug;56(8):B340-9. doi: 10.1093/gerona/56.8.b340.
Mutant mice with a combined deficiency of growth hormone (GH), prolactin, and thyrotropin, and knockout mice with GH resistance, live longer than their normal siblings. The extension of life span in these animals is very large (up to 65%), reproducible, and not limited to any particular genetic background or husbandry conditions. In addition to demonstrating that genes control aging in mammals, these findings suggest that GH actions, growth, and body size may have important roles in the determination of life span. We describe the key phenotypic characteristics of long-living mutant and knockout mice, with an emphasis on those characteristics that may be related to delayed aging in these animals. We also address the broader topic of the relationship between GH, growth, maturation, body size, and aging, and we attempt to reconcile the well-publicized antiaging action of GH with the evidence that suppression of GH release or action can prolong life.
生长激素（GH）、催乳素和促甲状腺激素联合缺乏的突变小鼠以及具有GH抗性的基因敲除小鼠，比它们的正常同胞寿命更长。这些动物的寿命延长幅度很大（高达65%），具有可重复性，且不限于任何特定的遗传背景或饲养条件。除了证明基因控制哺乳动物的衰老外，这些发现还表明GH的作用、生长和体型可能在寿命的决定中起重要作用。我们描述了长寿突变和基因敲除小鼠的关键表型特征，重点关注那些可能与这些动物衰老延迟相关的特征。我们还探讨了GH、生长、成熟、体型和衰老之间关系这一更广泛的话题，并试图调和广为人知的GH抗衰老作用与抑制GH释放或作用可延长寿命的证据之间的矛盾。
