Ghrelin does not mediate the somatotroph and corticotroph responses to the stimulatory effect of glucagon or insulin-induced hypoglycaemia in humans

Summary objective Acylated ghrelin, a gastric peptide, possesses a potent GH‐ but also significant ACTH/cortisol‐releasing activity mediated by the activation of GH secretagogue receptors (GHS‐R) at the hypothalamus–pituitary level. The physiological role of ghrelin in the control of somatotroph and corticotroph function is, however, largely unclear. Glucagon is known to induce a clear increase of GH, ACTH and cortisol levels in humans, at least after intramuscular administration. In fact, glucagon is considered to be a classical alternative to insulin‐induced hypoglycaemia (ITT) for the combined evaluation of the function of GH and the hypothalamus–pituitary–adrenal (HPA) axis. We aimed to clarify whether ghrelin mediate the GH and corticotroph responses to intramuscular glucagon or ITT, which has recently been reported able to induce a surprising ghrelin decrease. subjects To this aim we enrolled six normal young male subjects [age (mean ± SD): 29·0 ± 8·0 years, body mass index (BMI) 21·9 ± 2·5 kg/m2]. design and measurements In all the subjects we studied ghrelin, GH, ACTH, cortisol and glucose levels after glucagon (GLU; 0·017 mg/kg intramuscularly), ITT (0·1 IU/kg insulin intravenously) or saline administration. results Saline infusion was not followed by any significant variation in ghrelin, GH and glucose levels while ACTH and cortisol showed the expected spontaneous morning trend toward a decrease. GLU administration increased (P