Key result
Growth hormone secretagogues release GH directly from the pituitary and act centrally to activate hypothalamic neurones, requiring an intact GHRH system for potent in vivo activity.
GH secretagogues act through both pituitary and hypothalamic pathways to stimulate GH release, highlighting complex central mechanisms of action.
Should not yet inform clinical use of GH secretagogues; leaves open targeted mechanistic trials in intact GHRH states.
Various novel growth hormone (GH) secretagogues have been developed. GH secretagogues release GH directly from the pituitary via a pathway distinct from that involving GH-releasing hormone (GHRH). However, they also act centrally to activate hypothalamic neurones, and require an intact GHRH system for potent in vivo activity. Both normal and transgenic growth-retarded (Tgr) rats release GH in response to GH secretagogues, and their responses are sensitive to the pattern of secretagogue administration. GH secretagogues are not completely specific for GH release, but also activate the adrenocorticotrophin-adrenal axis, implying that they have additional central actions. The recent cloning of an endogenous receptor for GH secretagogues now makes it possible to identify central targets for their action. An endogenous receptor implies the existence of an endogenous ligand, but its site of production, relationship to the xenobiotic pharmacological agents and its underlying physiological relevance remain unclear.
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Icaf Robinson (1997) conducted a review in Growth hormone physiology. Growth hormone secretagogues was evaluated. Growth hormone secretagogues release GH directly from the pituitary and act centrally to activate hypothalamic neurones, requiring an intact GHRH system for potent in vivo activity.
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