Abstract

Growth hormone (GH) secretion is controlled by central and peripheral factors (1). The chief hypothalamic regulators of GH release are growth hormone releasing hormone (GHRH) and somatostatin (somatotropin release inhibiting hormone, SRIH). The finding of specific hypothalamic and pituitary receptors for the recently synthesized GH secretagogues (GHS) has led to the hypothesis of a third neuroendocrine pathway affecting GH secretion mediated by a still unidentified endogenous ligand for GHS receptors. A number of other neuroendocrine signals represented by neurotransmitters, neuropeptides and neurohormones may also intervene on the above hypophysiotropic hormones indirectly modulating GH secretion. Among the peripheral factors a pivotal role is played by the negative feedback exerted at both hypothalamic and pituitary levels by insulin-like growth factor I (IGF-I), the chief mediator of most biological actions of GH. GH is endowed with a relevant role in the regulation of body composition and energy expenditure, and thus it is not surprising that metabolic substrates (glucose, aminoacids and lipids) exert a feedback control on GH release. This chapter will mainly focus on the functional status of the GH-IGF-I axis in conditions of under-and overnutrition. In this context the effects of metabolic substrates on GH secretion as well as the influence exerted by GH on body composition and energy metabolism will be discussed.

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