Impaired growth hormone secretion associated with low glucocorticoid levels: an experimental model for the Giustina effe
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EDITORIAL
Impaired growth hormone secretion associated with low glucocorticoid levels: an experimental model for the Giustina effect Andrea Giustina • Gherardo Mazziotti
Received: 10 April 2014 / Accepted: 18 April 2014 Ó Springer Science+Business Media New York 2014
Hattori et al. [1] in this issue of Endocrine report on an interesting experimental model of dioxin-induced fetal growth retardation. This study found that oral administration of dioxin to pregnant rats reduced both the pituitary expression and serum levels of growth hormone (GH) in perinatal pups [1]. Concomitantly, dioxin decreased serum concentration of corticosterone in the studied model. Administration of physiological doses of corticosterone to dioxin-exposed mothers restored or tended to restore the dioxin-induced reduction of both GH expression and fetal body weight [1]. Taken together, these observations suggest that dioxin-induced fetal growth disorders are due, at least in part, to impaired GH expression and secretion in the presence of low circulating glucocorticoids [1]. GH is secreted in pulses by the pituitary gland. It is regulated by the hypothalamus via the stimulating factor GH-releasing hormone (GHRH) and the inhibitory hormone somatostatin [2]. In addition to classic hypothalamic peptides, many other neuropeptides (ghrelin and galanin), neurotransmitters (acetylcholine), metabolic substances (glucose and amino acids), and circulating hormones (thyroid and sex hormones) modulate GH production [2–6]. Regulation of GH secretion is deranged in many human diseases including Cushing syndrome [7–9]. In fact, glucocorticoids are among the most relevant circulating hormones acting as GH regulators with multiple effects at hypothalamic (increase somatostatin tone), pituitary (expression of GH and GHRH receptor), and peripheral level (decreased production of insulin-like
A. Giustina (&) G. Mazziotti University of Brescia, Poliambulatori di Via Biseo,Via Biseo 17, 25123 Brescia, Italy e-mail: [email protected]
growth factor 1, IGF-I, which is the peripheral mediator of GH action) [10, 11]. Interestingly, findings of Hattori et al. [1] are in agreement with data suggesting that glucocorticoids may be crucial for differentiation and maturation of somatotropes [12, 13]. Glucocorticoids can also enhance the GH response of somatotropes to GHRH and ghrelin as effect of enhanced expression of their receptors on pituitary cells [14–16]. In vivo studies suggest that glucocorticoids may both stimulate and inhibit GH secretion with the net biological effect related to hormonal levels and duration of exposure [10, 11]. In fact, as authors of the Endocrine paper correctly pointed out [1] although maternal co-treatment with corticosterone at low dose (1 mg/kg) restored defects produced by dioxin, higher doses such as 10 mg/kg corticosterone failed to produce beneficial effects on dioxin-exposed fetuses. In the adrenalectomized rat a blunted GH secretion in response to GHRH was observed while glucocorticoid replacement restored GH secretion to norm
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