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Orchiectomy Markedly Reduces the Concentration of the Three Isoforms of Transforming Growth Factor ß in Rat Bone, and Reduction Is Prevented by Testosterone¹

Departments of Medicine and Pharmacology (R.K.G., N.H.B.), Medical University of South Carolina and Department of Veterans Affairs Medical Center, Charleston, South Carolina 29401-5799; Department of Orthopaedics (R.T.T.), Mayo Clinic, Rochester, Minnesota 55905; and Department of Physiologic Sciences (T.J.W.), University of Florida College of Veterinary Medicine, Gainesville, Florida 32610

Address all correspondence and requests for reprints to: Norman H. Bell, M.D., Veterans Affairs Medical Center, 109 Bee Street, Charleston, South Carolina 29401-5799.

Available evidence indicates that transforming growth factor ß (TGFß) is produced by bone cells, that production is enhanced by testosterone and dihydrotestosterone, and that TGFß is an important modulator of bone formation, induction, and repair. To determine the relative concentrations of isoforms of skeletal TGFß, whether orchiectomy alters the concentration of TGFß in long bones, and whether alteration is prevented by testosterone replacement, male Sprague-Dawley rats were either sham-operated and given placebo (n = 20) or orchiectomized and given either placebo (n = 20) or 100 mg testosterone (n = 20) by slow-release pellets implanted sc at the back of the neck and killed at 6 weeks. Orchiectomy did not change serum calcium and lowered serum testosterone and serum phosphorus; these reductions were prevented by testosterone replacement. TGFß₁ in skeletal extracts was much more abundant than TGFß₂ or TGFß₃. Orchiectomy reduced skeletal TGFß by over 80 percent, and reduction was prevented by testosterone replacement. The relative abundance of the three isoforms of TGFß in bone was not influenced by orchiectomy or testosterone replacement, and skeletal messenger RNA of TGFß₁ and TGFß₂ was not altered 4 weeks after orchiectomy. Messenger RNA for TGFß₃ was below the limits of detection. Thus, testosterone deficiency markedly diminishes skeletal TGFß, and reduction is prevented by testosterone replacement. The findings support the hypothesis that testosterone and TGFß are required for maintenance of the skeleton in male rats.

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