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

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...

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Published in:Endocrinology (Philadelphia) 2003-06, Vol.144 (6), p.2553-2558
Main Authors: Rooman, Raoul P. A, Kuijpers, Gilliam, Gresnigt, Ria, Bloemen, Ruud, Koster, Johanna G, van Buul-Offers, Sylvia C
Format: Article
Language:English
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Summary: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
ISSN:0013-7227
1945-7170
DOI:10.1210/en.2003-0062