Bone

Abstract

The effects of GH and IGF-1 on somatic growth have been closely linked since the somatomedin hypothesis was proposed over 50 years ago (Salmon and Daughaday 1957). However, it has also been established that GH exerts its direct effects independent of IGF-1 mediation in the regulation of growth. Furthermore, roles of estrogen and androgen on bone growth have been elucidated using GHR-/- mice. Androgens stimulate bone formation independent of systemic or local IGF-1 production. Estradiol, on the other hand, upregulates systemic IGF-1 levels by stimulating hepatic IGF-1 synthesis independent of GH. Thus, estrogen or androgen action might be clinically useful on bone modeling for patients with age-dependent GH-IGF-1 deficiency and/or GH-resistant conditions. Since the contributions of GH and IGF-1 as well as other hormones are complex, the generation of temporal or bone-specific GHR knockout mice will be valuable to further characterize the contribution of GH in bone growth. © Springer-Verlag Berlin Heidelberg 2011.