The skeletal structure of insulin-like growth factor I-deficient mice
The skeletal structure of insulin-like growth factor I-deficient mice
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DOI：
10.1359/jbmr.2001.16.12.2320
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发表时间：
2001-12-01
影响因子：
6.2
通讯作者：
Halloran, B
中科院分区：
文献类型：
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作者：
Bikle, D;Majumdar, S;Halloran, B
胰岛素样生长因子I（IGF-I）对生长的重要性已得到充分证实。然而，骨骼上IGF-I的缺乏还没有得到彻底的检查。因此，我们使用组织形态计量学、外周定量计算机断层扫描（pQCT）和微计算机断层扫描（mu CT）分析了同源重组（敲除[k/o]）导致IGF-I缺陷的小鼠骨的结构特性。在研究时（4个月），k/o小鼠的大小是其野生型同窝小鼠的24%。k/o胫骨为野生型骨骼的28%，L1椎骨为野生型骨骼的26%。k/o胫骨的骨形成率（BFR）为野生型同窝仔的27%。就BFR而言，k/o骨对生长激素（GH;增加1.7倍）的反应正常，对IGF-I（增加5.2倍）的反应超正常。在k/o小鼠中，胫骨近端的皮质厚度减少了17%。然而，与野生型对照组相比，k/o小鼠的骨小梁体积（骨体积/总体积[BV/TV]）增加了23%（雄性小鼠）和88%（雌性小鼠），这是由于骨小梁的连接性增加、数量增加和间距减少。这些变化在L1中较少或未发现。因此，IGF-I的缺乏导致骨骼结构的发展，尽管较小，但显得更紧凑。
The importance of insulin-like growth factor I (IGF-I) for growth is well established. However, the lack of IGF-I on the skeleton has not been examined thoroughly. Therefore, we analyzed the structural properties of bone from mice rendered IGF-I deficient by homologous recombination (knockout [k/o]) using histomorphometry, peripheral quantitative computerized tomography (pQCT), and microcomputerized tomography (mu CT). The k/o mice were 24% the size of their wild-type littermates at the time of study (4 months). The k/o tibias were 28% and L1 vertebrae were 26% the size of wild-type bones. Bone formation rates (BFR) of k/o tibias were 27% that of the wild-type littermates. The k/o bones responded normally to growth hormone (GH; 1.7-fold increase) and supranormally to IGF-I (5.2-fold increase) with respect to BFR. Cortical thickness of the proximal tibia was reduced 17% in the k/o mouse. However, trabecular bone volume (bone volume/total volume [BV/TV]) was increased 23% (male mice) and 88% (female mice) in the k/o mice compared with wild-type controls as a result of increased connectivity, increased number, and decreased spacing of the trabeculae. These changes were either less or not found in L1. Thus, lack of IGF-I leads to the development of a bone structure, which, although smaller, appears more compact.