In Vivo Modulation of Somatomedin Receptor Sites: Effects of Growth Hormone Treatment of Hypopituitary Children*

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Abstract
We have previously demonstrated that somatomedin (SM) can induce the loss of specific SMC receptors on cultured IM-9 lymphocytes in a time-and concentration-dependent manner. To investigate the acute regulation of SM binding under in vivo conditions, we have evaluated SM receptors on circulating mononuclear cells obtained from 12 hypopituitary dwarfs before and after 4 days of human GH administration (0.1 U/kg·day). Plasma SM glevels, measured by radioreceptor assay, rose from 0.37 ±0.08 U/ml (mean ±SEM) to 1.00 ±0.10 (P < 0.001). Concomitantly, specific binding of [125I]SMC to 50 × 106 mononuclear cells/ml fell from 13.61± 0.97% to 10.40 ± 0.85% (P < 0.02). The decrease in specific binding was predom predominantly secondary to a reduced number of SMC receptor sites per cell, with no alteration in receptor affinity. Overall, a significant inverse correlation was observed between plasma SM levels and mononuclear cellular binding of [125I]SMC (P < 0.001). The data demonstrate that treatment of hypopituitary dwarfs with conventional therapeutic doses of human GH results in significant acute increases in plasma SM levels in the majority of subjects, with a reciprocal decline in the specific binding of [125I]SMC. We,conclude that SM, like insulin, is capable of regulating homologous receptor concentrations under both in vitro and in vivo conditions.

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