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Pituitary Research Unit (K-CL, GML, KKYH), Garvan Institute of Medical Research, and Department of Endocrinology (KKYH), St Vincent's Hospital, Sydney, New South Wales, Australia; Research Centre for Endocrinology and Metabolism (GJ), Sahlgrenska University Hospital, Göteborg, Sweden.
* To whom correspondence should be addressed.
Growth hormone (GH) plays a pivotal role in regulating body growth and development, which is modulated by sex steroids. A close interplay between estrogen and GH leads to attainment of gender-specific body composition during puberty. The physiological basis of the interaction is not well understood. Most previous studies have focused on estrogen effects on GH secretion. There is also strong evidence that estrogen modulates GH action independent of secretion. Oral but not transdermal administration of estrogen impairs the metabolic action of GH in the liver, causing a fall in IGF-I production and fat oxidation. This results in a loss of lean tissue and a gain of body fat in post-menopausal women and an impairment of GH effect in hypopituitary women on GH replacement. The negative metabolic sequelae are potentially important because of the widespread use of oral estrogen and estrogen-related compounds.
Estrogen affects GH action at the level of receptor expression and signaling. More recently, estrogen has been shown to inhibit JAK/STAT signaling by GH via the induction of SOCS-2, a protein inhibitor for cytokine signaling. This represents a novel paradigm of steroid regulation of cytokine receptors, and is likely to have significance for a diverse range of cytokine function.
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