| pubmed-article:20938222 | pubmed:abstractText | IGF-I and PTH have synergistic actions on bone and some effects of the anabolic actions of PTH are mediated by local production of IGF-I, as has been shown in vitro and in vivo studies both in animals and humans. PTH can induce skeletal IGF-I expression both in vitro and in vivo. In chondrocytes, IGF-I synthesis is under GH control, whereas in osteoblasts its synthesis is fundamentally under the control of PTH. PTH stimulates the synthesis of IGF-I via a cAMP-dependent mechanism, and this factor has pro-differentiating and prosurvival effects on osteoblasts. In in vitro studies, IGF-I and PTH have shown a synergistic action on the osteoblasts of bone marrow. Human clinical data confirm the interactions between PTH and GH-IGF-I axis on bone. PTH is involved in the development of osteoporosis in adult patients with GH deficiency (GHD). In fact, patients with GHD show renal, skeletal, and intestinal cell insensitivity to PTH, leading to a mild state of PTH resistance and increased serum PTH levels. In addition, GH replacement in these patients restores PTH secretory rhythm, increases bone turnover markers, 1,25-dihydroxy vitamin D concentration, and Ca absorption/reabsorption, thus contributing to the positive effects of GH on bone. On the other hand, in post-menopausal women with primary hyperparathyroidism a reduced secretion of GH is observed, in association with a greater impairment of bone mass. GH administration resulted in increased IGF-I concentration, decreased PTH concentration, and increased nephrogenous cAMP. In conclusion, the anabolic action of PTH requires paracrine and autocrine effects of IGF-I. | lld:pubmed |
