Abstract
There is growing evidence that both endogenous as well as exogenous steroids augment growth hormone (GH) synthesis and secretion. In men, as well as women, basal and stimulated GH levels correlate with circulating estrogen levels under a variety of circumstances. To further support this hypothesis, there are a number of specific clinical examples. First, a significant increase in GH secretion occurs during normal and precocious pubertal development (1–3). Second, in girls with Turner syndrome, pulsatile GH activity is augmented during estrogen treatment (4). Third, postmenopausal women treated with exogenous estrogens have increased basal and growth hormone-releasing hormone-stimulated GH secretion (5). Finally, basal plasma GH levels rise in men treated with estrogens and fall to basal levels after cessation of therapy (6). In contrast, gonadotropin-releasing hormone (GnRH) agonists typically suppress estrogen production and inhibit GH release in women with endometriosis or leiomyomas, as well as in children treated with GnRH agonists for precocious puberty (7,8).
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References
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Carr, B.R. (1999). Growth Hormone Axis Response to Superovulation. In: Veldhuis, J.D., Giustina, A. (eds) Sex-Steroid Interactions with Growth Hormone. Proceedings in the Serono Symposia USA Series. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-1546-2_8
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DOI: https://doi.org/10.1007/978-1-4612-1546-2_8
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