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Dexamethasone Differentially Inhibits Thyroxine- or Growth Hormone-Induced Body and Organ Growth of Snell Dwarf Mice

Department of Pediatric Endocrinology, University Medical Center, 3508 AB Utrecht, The Netherlands

Address all correspondence and requests for reprints to: Raoul Rooman, M.D., Department of Pediatrics, Antwerp University Hospital, Wilrijkstraat 10, B-2650 Edegem, Belgium. E-mail: raoul.rooman{at}uza.be.

Supraphysiological doses of glucocorticoids cause growth retardation in both animals and humans. Many studies have addressed the interaction of glucocorticoids with the GH/IGF system, but little is known about the effect of glucocorticoids on T₄-stimulated growth. The Snell dwarf mouse is deficient in GH, thyroid-stimulating hormone, and prolactin and therefore allows the study of the effect of glucocorticoids on the growth induced by GH and T₄ without their mutual interaction. Four weeks of treatment with T₄ (1 µg/d) or human GH (50 mU/d) equally increased nose-tail length (3.1 ± 0.1 cm and 3.0 ± 0.2 cm, respectively). Dexamethasone (DXM) had much less impact on T₄-stimulated growth than on GH-induced growth (T₄ + DXM: 2.4 ± 0.1 cm vs. GH+ DXM: 1.4 ± 0.1 cm). Similar data were obtained for body weight gain. T4 and GH had a different effect on the weight of various organs: GH caused a higher increase in liver and lumbar vertebrae weight, and T₄ was a better stimulator for kidney (P < 0.05), thymus, and spleen growth. Remarkably, T₄-stimulated growth of the organs was less affected by DXM than GH-induced organ growth. GH even potentiated the growth inhibition by DXM in the thymus and tibia. In conclusion, T₄-stimulated growth in Snell dwarf mice is less affected by DXM than growth stimulated by GH

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