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The Somatostatin Analog Octreotide Inhibits GH-Stimulated, But Not IGF-I-Stimulated, Bone Growth in Hypophysectomized Rats

Division of Endocrinology and Diabetes, Department of Internal Medicine, University Hospital Zurich (J.Z., M.G.-P.), 8091 Zurich, Switzerland; Novartis Pharma, Preclinical Research (G.W.), 4002 Basel, Switzerland; M. E. Müller Institute of Biomechanics, University of Bern (E.B.H.), 3010 Bern, Switzerland; and Division of Neuroendocrinology, Institute of Anatomy, University of Zurich (M.R.), 8057 Zurich, Switzerland

Address all correspondence and requests for reprints to: Jürgen Zapf, M.D., Division of Endocrinology and Diabetes, Department of Internal Medicine, University Hospital, 8091 Zurich, Switzerland. E-mail: . ndozaj{at}usz.unizh.ch

IGF-I mediates growth-promoting actions of GH. In the present study we investigated whether the somatostatin analog octreotide blunts the stimulatory effects of GH and/or IGF-I on bone growth in hypophysectomized rats infused for 6 d with vehicle, GH, or IGF-I. We found that octreotide significantly suppressed the GH-induced rise in liver IGF-I mRNA (-27%) and peptide (-32%) and the serum IGF-I level (-26%) and concomitantly inhibited GH-stimulated, but not IGF-I-stimulated, body weight gain (-31%), tibial epiphyseal width (-14%), and bone growth rate (-24%). Furthermore, octreotide significantly reduced the GH-induced increase in the number of IGF-I immunoreactive chondrocytes in all layers (except in the upper hypertrophic zone) of the tibial growth plate cartilage (P < 0.0001 for stem cell and proliferative zone; P < 0.0005 for lower hypertrophic zone). These findings demonstrate that octreotide does not interfere with IGF-I action, but does interfere with local GH-stimulated IGF-I production in the growth plate. Thus, besides inhibiting pituitary GH secretion, octreotide exerts inhibitory peripheral effects on GH-stimulated longitudinal bone growth.

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