GROWTH-HORMONE RESPONSE TO GROWTH HORMONE-RELEASING HORMONE (GHRH), INSULIN, CLONIDINE AND ARGININE AFTER GHRH PRETREATMENT IN OBESE CHILDREN - EVIDENCE OF SOMATOSTATIN INCREASE

To clarify the possible neuroendocrine mechanisms underlying the impai rment in growth hormone (GH) secretion present in obesity, the GH resp onse to GH-releasing hormone (GHRH, N = 6), insulin hypoglycemia (N = 6), clonidine (N = 7) and arginine (N = 8) after GHRH pretreatment (1 mu g/kg iv 2 h before the tests) was evaluated in 27 obese peripuberta l children and in a group of normal-weight short-normal children (N = 26). Growth hormone-releasing hormone pretreatment and all further sti muli elicited a statistically significant GH response in both obese an d short-normal children; in the latter group arginine did not induce a significant GH response. No differences were found among the GH respo nses after the second stimuli in obese children, while in short-normal children the arginine peak and area values were lower than after GHRH and clonidine, Comparison between the two groups showed similar basel ine but higher stimulated GH levels in normal-weight children after al l tests except ariginine, after which no difference was present. In co nclusion, the neuroregulation of GH release seems to be similar qualit atively in normal-weight and obese youngsters; the different behavior observed after arginine, which is supposed to act through somatostatin inhibition, might be due to a chronic increase in somatostatinergic t one responsible for the lower stimulated GH levels in obesity.