期刊
EXPERIMENTAL GERONTOLOGY
卷 46, 期 2-3, 页码 108-111出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exger.2010.08.020
关键词
Longevity; Cancer; Insulin-like growth factor 1 (IGF-1); Dwarf mice
资金
- NIA NIH HHS [P01 AG031736, R01 AG019899, R21 AG038850] Funding Source: Medline
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. (C) 2010 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据