Growth hormone enhances hepatic epidermal growth factor receptor concentration in mice.

J O Jansson; S Ekberg; S B Hoath; W G Beamer; L A Frohman

doi:10.1172/JCI113804

Division of Endocrinology, University of Cincinnati College of Medicine, Ohio 45267.

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Division of Endocrinology, University of Cincinnati College of Medicine, Ohio 45267.

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Division of Endocrinology, University of Cincinnati College of Medicine, Ohio 45267.

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Division of Endocrinology, University of Cincinnati College of Medicine, Ohio 45267.

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Division of Endocrinology, University of Cincinnati College of Medicine, Ohio 45267.

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Published in Volume 82, Issue 6 on December 1, 1988
J Clin Invest. 1988;82(6):1871–1876. https://doi.org/10.1172/JCI113804.
© 1988 The American Society for Clinical Investigation

Published December 1, 1988 - Version history

The effect of growth hormone (GH) on binding of epidermal growth factor (EGF) to liver membrane preparations was investigated in hypophysectomized mice and partially GH-deficient, genetic mutant "little" (lit/lit) mice. The EGF binding of normal male mice and testosterone-treated females was higher than in normal females. Due to diminished receptor concentration, hepatic EGF binding was decreased in male and female lit/lit mice to a level that was unaffected by gender or androgen treatment. GH replacement therapy by intermittent injections and continuous infusion restored the EGF binding of hypophysectomized mice to normal male and female levels, respectively, suggesting a role for the more pulsatile GH secretion in normal males. In lit/lit mice, however, both continuous and intermittent GH resulted in EGF binding levels comparable to those in normal females. In normal males continuous GH suppressed EGF binding. In conclusion, endogenous GH secretion induces EGF receptors in mice and this effect may be modulated by sex differences in GH secretion.