| First Author | Bikle D | Year | 2001 |
| Journal | J Bone Miner Res | Volume | 16 |
| Issue | 12 | Pages | 2320-9 |
| PubMed ID | 11760848 | Mgi Jnum | J:112522 |
| Mgi Id | MGI:3656446 | Doi | 10.1359/jbmr.2001.16.12.2320 |
| Citation | Bikle D, et al. (2001) The skeletal structure of insulin-like growth factor I-deficient mice. J Bone Miner Res 16(12):2320-9 |
| abstractText | 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 (muCT). 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. |
