A general IGF-I overexpression effectively rescued somatic growth and bone deficiency in mice caused by growth hormone receptor knockout
A general IGF-I overexpression effectively rescued somatic growth and bone deficiency in mice caused by growth hormone receptor knockout
复制标题
IGF-I 的普遍过度表达可有效挽救因生长激素受体敲除引起的小鼠体细胞生长和骨质缺乏
DOI：
10.3109/08977190903299270
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发表时间：
2009-11
期刊：
影响因子：
1.8
通讯作者：
Xiao Wang
中科院分区：
文献类型：
--
作者：
Xiao Wang
Both growth hormone and insulin-like growth factor (IGF)-I are essential for postnatal somatic growth, while exerting distinct effects on energy homeostasis. Although growth hormone controls IGF-I production, whether IGF-I was the exclusive mediator of its growth promotion is still debated. In order to further explore their in vivo interactions in somatic growth as well as in energy homeostasis, we have crossed mutant (MT-IGF) transgenic mice onto the GHR − / − background. As expected, GHR gene deficiency caused growth retardation, including significant decreases in lumbar, femur and total body lengths, as well as decreased bone area, mineral content and mineral density. IGF-I overexpression alone in MT-IGF mice increased the weight, with no significant change in bone mineralization or longitudinal growth. Compared to GHR − / − littermates, overexpressed IGF-I in bitransgenic mice (GHR − / − and MT-IGF positive) exhibited fully restored body weight, lumbar (but not femur) and total body lengths, and normalized overall bone area, mineral content and density. On the other hand, there were significant changes in fasting glucose level, glucose tolerance, lean/fat masses and even adipose histology as a result of the transgenic/knockout double-crossing. IGF-I overexpression normalized glucose tolerance in GHR − / − mice. Intriguingly, on GHR+/ − background of partial growth hormone insensitivity, overexpression of IGF-I caused a significant weight gain. Our results thus establish that the growth defect and bone deficiency caused by lack of growth hormone signaling can be effectively restored by increasing IGF-I production in vivo.
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影响因子：
4.8
作者：
Wu, YingJie;Sun, Hui;LeRoith, Derek
通讯作者：
LeRoith, Derek
影响因子：
10.5
作者：
POWELLBRAXTON, L;HOLLINGSHEAD, P;STEWART, TA
通讯作者：
STEWART, TA
DOI：
10.1016/j.ghir.2005.12.001
发表时间：
2006-02
期刊：
Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society
影响因子：
--
作者：
Z. Laron,;S. Ginsberg;P. Lilos;Mira Arbiv;N. Vaisman
通讯作者：
Z. Laron,;S. Ginsberg;P. Lilos;Mira Arbiv;N. Vaisman
影响因子：
29.4
作者：
Ohneda, K;Ulshen, MH;Lund, PK
通讯作者：
Lund, PK
影响因子：
4.8
作者：
K. Wallenius;Klara Sjo Gren;Xiao-ding Peng;Seungjoon Park;V. Wallenius;Jun-li Liu;M. Umaerus;H. Wennbo;O. Isaksson;L. Frohman;R. Kineman;C. Ohlsson;J. Jansson
通讯作者：
K. Wallenius;Klara Sjo Gren;Xiao-ding Peng;Seungjoon Park;V. Wallenius;Jun-li Liu;M. Umaerus;H. Wennbo;O. Isaksson;L. Frohman;R. Kineman;C. Ohlsson;J. Jansson