Endocrine Abstracts

Growth hormone (GH) secretion is regulated by a complex interplay between GH-releasing hormone (GHRH), somatostatin and several other central and peripheral modulatory signals. Ghrelin has been hypothesized as physiological amplifier of GH pulsatility and acts via mechanisms, at least partially, independent of GHRH and somatostatin. The GH response to GHRH is strongly inhibited by previous administration of recombinant human GH (rhGH), likely as a consequence of a somatostatin-mediated negative GH auto-feedback. The effect of exogenous rhGH on the GH-releasing effect of ghrelin has never been tested so far. In 5 normal young volunteers we studied the acute GH response to ghrelin (2.0 mcg/kg iv at 0 min) during saline or rhGH infusion (4.0 μg/Kg/h i.v. from −180 min to +60 min). Mean GH levels during saline infusion were: 0.7±0.4 mcg/l. The rhGH administration increased mean GH levels to: 22.1±2.3 mcg/l (P<0.01). During saline, ghrelin administration induced clear cut increase of GH secretion (Δpeak: 55.0±6.7 mc/l; ΔAUC: 2096.4±193.2 mcg/l/h; P<0.01 vs baseline). During rhGH infusion, ghrelin elicited the same potent GH-releasing effect (Δpeak: 92.2±53.4 mcg/l; ΔAUC: 2298.3±684.4 mcg/l/h; P<0.01). In conclusion, these results show that the acute rhGH administration does not modify the GH-releasing action of ghrelin. As GH auto-feedback is known to act by a concomitant reduction in the activity of GHRH-secreting neurons and increase of somatostatinergic tone, these data further indicate that the impact of the ghrelin system on somatotroph function is remarkably independent of either GHRH or somatostatin.