Corticosteroid‐induced growth hormone secretion in normal and obese subjects

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Abstract
SUMMARY: objective In normal subjects, cortlcosterolds stimulate growth hormone (GH) secretion at 3 hours. Obesity is associated with blunted GH secretion. In order to clarify both the deranged mechanism of GH secretion In obesity and the corticosterold mechanism of action we have assessed In normal and obese subjects the effects of dexamethasone, pyridostigmine (a drug capable of suppressing somatostatln release) and GHRH. We also compared in normal subjects the stimulatory effect of three different cortlcosterolds on plasma GH levels design In both normal and obese subjects the following tests were carried out: placebo; dexamethasone alone (4 mg l.v. at 0 minutes); and dexamethasone plus pyridostigmine (120 mg p.o. at 60 minutes)In normal subjects we also studied the effects of hydrocortisone (100 mg l.v. at 0 minutes) and deflazacort (a corticosteroid that does not cross the blood‐brain barrier) (60 mg l.v. at 0 minutes). In obese subjects we also assessed the effect of dexamethasone plus GHRH (100 μ g l.v. at 150 minutes) on plasma GH levels. patients Ten normal subjects and 22 obese subjects were studied. Normal controls were within 10% of their ideal body weight. Obese subjects had a body mass Index of 37·1±1·1 (mean ± SEM) measurements Plasma GH levels were measured by radioimmunoassay. results Dexamethasone‐induced GH secretion In normal subjects (28·6±7·8 mμ/l, P > 0·05). Cortlcosterolds did not alter GH levels In obese subjects. Pretreatment with pyridostigmine increased dexamethasone‐induced GH release in normal subjects (40·8±6·8 mμ/l) but this did not achieve statistical significance. Dexamethasone plus pyridostigmine did not alter GH levels In obese subjects (8·0±1·6 mU/l). In some subjects, dexamethasone protreatment potentiated GHRH‐stimulated GH secretion, while In half the subjects the basal GH levels were not altered.In control subjects, hydrocortisone and deflazacort caused GH release similar to dexamethasone conclusions Corticosteroids are a new and selective stimulus of GH secretion. They do not cause GH release in obese subjects. Their relative independence from chollnergic control suggest that they act by reducing somatostatin secretion