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Increased serum and bone matrix levels of transforming growth factor {beta}1 in patients with GH deficiency in response to GH treatment.

Author(s): Ueland T, Lekva T, Otterdal K, Dahl TB, Olarescu NC, Jorgensen AP, Fougner KJ, Brixen K, Aukrust P, Bollerslev J

Affiliation(s): Research Institute for Internal Medicine Department of Endocrinology Section of Clinical Immunology and Infectious Faculty of Medicine, Oslo University Hospital Rikshospitalet, University of Oslo, Oslo, Norway. thor.ueland@medisin.uio.no

Publication date & source: 2011-09, Eur J Endocrinol., 165(3):393-400. Epub 2011 Jun 8.

Publication type: Randomized Controlled Trial; Research Support, Non-U.S. Gov't

OBJECTIVE: Patients with adult onset GH deficiency (aoGHD) have secondary osteoporosis, which is reversed by long-term GH substitution. Transforming growth factor beta1 (TGFbeta1 or TGFB1) is abundant in bone tissue and could mediate some effects of GH/IGFs on bone. We investigated its regulation by GH/IGF1 in vivo and in vitro. DESIGN AND METHODS: The effects of GH substitution (9-12 months, placebo controlled) on circulating and cortical bone matrix contents of TGFbeta1 were investigated in patients with aoGHD. The effects of GH/IGF1 on TGFbeta1 secretion in osteoblasts (hFOB), adipocytes, and THP-1 macrophages as well as the effects on release from platelets were investigated in vitro. RESULTS: In vivo GH substitution increased TGFbeta1 protein levels in cortical bone and serum. In vitro, GH/IGF1 stimulation induced a significant increase in TGFbeta1 secretion in hFOB. In contrast, no major effect of GH/IGF1 on TGFbeta1 was found in adipocytes and THP-1 macrophages. Finally, a minor modifying effect on SFLLRN-stimulated platelet release of TGFbeta1 was observed in the presence of IGF1. CONCLUSION: GH substitution increases TGFbeta1 in vivo and in vitro, and this effect could contribute to improved bone metabolism during such therapy, potentially reflecting direct effect of GH/IGF1 on bone cells.

Page last updated: 2011-12-09

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