HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (16) Citing Articles via Google Scholar Google Scholar Articles by Ueland, T. Search for Related Content PubMed PubMed Citation Articles by Ueland, T.

GH/IGF-I and bone resorption in vivo and in vitro

¹ Section of Endocrinology and ² Research Institute for Internal Medicine, Rikshospitalet University Hospital, N-0027 Oslo, Norway

(Correspondence should be addressed to T Ueland; Email: thor.ueland{at}medisin.uio.no)

Abstract

IGF-I may act as one of several coupling agents by activating bone formation and bone resorption. In vivo studies in normal subjects, postmenopausal women and patients with excess or diminished GH production (acromegaly and GHD) indicate that both GH and IGF-I activate osteoclasts, but that GH has a more pronounced effect, independently of IGF-I. In vitro, GH and IGF receptors have been demonstrated on osteoclasts and both GH and IGF-I may directly modify osteoclast function and activity. In addition to direct effects on osteoclasts, GH and IGF-I may affect bone resorption indirectly by stimulating release of paracrine mediators that regulate osteoclastic resorption (cytokines). Critical for the bone resorptive process is the balance between OPG and RANKL, which is regulated by many systemic factors. In vivo and in vitro, GH/IGF-I may modulate this balance but these studies are difficult to interpret, reflecting the complexity of this system. Increased OPG expression may possibly protect against GH/IGF-I-induced bone resorption and potentially be important for the long-term beneficial effects of GH replacement. Further studies investigating the OPG/RANKL ratio and system in experimental and transgenic GH/IGF models may clarify these issues.

This article has been cited by other articles:

				K. E. Govoni, J. E. Wergedal, L. Florin, P. Angel, D. J. Baylink, and S. Mohan Conditional Deletion of Insulin-Like Growth Factor-I in Collagen Type 1{alpha}2-Expressing Cells Results in Postnatal Lethality and a Dramatic Reduction in Bone Accretion Endocrinology, December 1, 2007; 148(12): 5706 - 5715. [Abstract] [Full Text] [PDF]

				V. Tangpricha, M. Luo, C. Fernandez-Estivariz, L. H. Gu, N. Bazargan, J.-M. Klapproth, S. V. Sitaraman, J. R. Galloway, L. M. Leader, and T. R. Ziegler Growth Hormone Favorably Affects Bone Turnover and Bone Mineral Density in Patients With Short Bowel Syndrome Undergoing Intestinal Rehabilitation JPEN J Parenter Enteral Nutr, November 1, 2006; 30(6): 480 - 486. [Abstract] [Full Text] [PDF]

				S. O. Akintoye, M. H. Kelly, B. Brillante, N. Cherman, S. Turner, J. A. Butman, P. G. Robey, and M. T. Collins Pegvisomant for the Treatment of gsp-Mediated Growth Hormone Excess in Patients with McCune-Albright Syndrome J. Clin. Endocrinol. Metab., August 1, 2006; 91(8): 2960 - 2966. [Abstract] [Full Text] [PDF]

				E. Cecconi, M. Gasperi, M. Genovesi, F. Bogazzi, L. Grasso, F. Cetani, M. Procopio, C. Marcocci, L. Bartalena, and E. Martino The reduction of bone mineral density in postmenopausal women with primary hyperparathyroidism is higher in the presence of concomitant GH secretion impairment. Eur. J. Endocrinol., July 1, 2006; 155(1): 41 - 45. [Abstract] [Full Text] [PDF]