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The Journal of Clinical Endocrinology & Metabolism Vol. 83, No. 1 81-87
Copyright © 1998 by The Endocrine Society


Original Studies

Effects of Short-Term Insulin-Like Growth Factor-I (IGF-I) or Growth Hormone (GH) Treatment on Bone Metabolism and on Production of 1,25-Dihydroxycholecalciferol in GH-Deficient Adults1

Tarcisio Bianda, Yvonne Glatz, Roger Bouillon, Ernst Rudolf Froesch and Christoph Schmid

Division of Endocrinology and Metabolism (T.B., Y.G., E.R.F., C.S.), Department of Internal Medicine, University Hospital, CH-8091 Zürich, Switzerland; Laboratorium voor Experimentele Geneeskunde en Endocrinologie (R.B.), Katholieke Universiteit Leuven, B-3000 Leuven, Belgium

Address correspondence and reprint requests to: Dr. Tarcisio Bianda, Division of Endocrinology and Metabolism, Department of Internal Medicine, University Hospital, CH-8091 Zürich, Switzerland.

Administration of insulin-like growth factor-I (IGF-I) or growth hormone (GH) is known to stimulate bone turnover and kidney function. To investigate the effects of IGF-I and GH on markers of bone turnover, eight adult GH-deficient patients (48 ± 14 yr of age) were treated with IGF-I (5 µg/kg/h in a continuous sc infusion) and GH (0.03 IU/kg/daily sc injection at 2000 h) in a randomized cross-over study. We monitored baseline values for three consecutive days before initiating the five-day treatment period, as well as the wash-out period of ten weeks. Serum osteocalcin, carboxyterminal and aminoterminal propeptide of type I procollagen (PICP and PINP, respectively) increased significantly within 2–3 days of both treatments (P < 0.02) and returned to baseline levels within one week after the treatment end. The changes in resorption markers were less marked as compared with formation markers. Total 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) rose significantly, whereas PTH and calcium levels remained unchanged during either treatment. Conclusions: Because the rapid increase in markers of bone formation was not preceded by an increase in resorption markers, IGF-I is likely to stimulate bone formation by a direct effect on osteoblasts. Moreover, because PTH, calcium, and phosphate remained unchanged, IGF-I appears to stimulate renal 1{alpha}-hydroxylase activity in vivo.




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