Growth hormone, insulin and aging: the benefits of endocrine defects.
Growth hormone, insulin and aging: the benefits of endocrine defects.
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DOI：
10.1016/j.exger.2010.08.020
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发表时间：
2011-02
影响因子：
3.9
通讯作者：
Bartke, Andrzej
中科院分区：
文献类型：
--
作者：
Bartke, Andrzej
小鼠的寿命可以通过自发或实验诱导的突变来延长，这些突变可以干扰生长激素（GH）、胰岛素样生长因子1 （IGF-1）或脂肪组织中胰岛素的生物合成或作用。生长激素抵抗和生长激素缺乏（以及促甲状腺素和催乳素）对衰老和寿命的影响是这些突变中最明显和最确定的。将这些内分泌缺陷与延缓衰老和延长寿命联系起来的潜在机制包括抗逆性增强、胰岛素和哺乳动物雷帕霉素靶蛋白（mTOR）信号的改变以及代谢调节。从长寿小鼠突变体的极端表型推断出的生理关系似乎广泛适用，包括基因正常（“野生型”）小鼠和其他哺乳动物物种。生长激素在控制人类衰老中的作用一直备受争议，但最近的数据表明，减少的促生长信号可以预防癌症和其他与年龄相关的疾病，并可能促进老年生存。
Longevity of mice can be increased by spontaneous or experimentally induced mutations that interfere with the biosynthesis or actions of growth hormone (GH), insulin-like growth factor 1 (IGF-1), or insulin in the adipose tissue. The effects of GH resistance and deficiency of GH (along with thyrotropin and prolactin) on aging and lifespan are the most pronounced and best established of these mutations. Potential mechanisms linking these endocrine deficits with delayed aging and extended longevity include increased stress resistance, alterations in insulin and mammalian target of rapamycin (mTOR) signaling and metabolic adjustments. Physiological relationships deduced from the extreme phenotypes of long-lived mouse mutants appear to apply broadly, encompassing genetically normal (“wild-type”) mice and other mammalian species. The role of GH in the control of human aging continues to be hotly debated, but recent data indicate that reduced somatotropic signaling provides protection from cancer and other age-related diseases and may promote old age survival.
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生长激素受体的破坏可防止卡路里的限制改善胰岛素作用和寿命。
影响因子：
3.7
作者：
Bonkowski MS;Dominici FP;Arum O;Rocha JS;Al Regaiey KA;Westbrook R;Spong A;Panici J;Masternak MM;Kopchick JJ;Bartke A
通讯作者：
Bartke A
影响因子：
4.8
作者：
Al-Regaiey, KA;Masternak, MM;Bartke, A
通讯作者：
Bartke, A
影响因子：
56.9
作者：
Conti, Bruno;Sanchez-Alavez, Manuel;Bartfai, Tamas
通讯作者：
Bartfai, Tamas
影响因子：
2.9
作者：
Rollo, CD
通讯作者：
Rollo, CD
影响因子：
2.9
作者：
Hunter, WS;Croson, WB;Meliska, CJ
通讯作者：
Meliska, CJ