Search

OBJECTIVE The aim of the present study was to measure dehydroepiandrosterone-sulphate (DHEA-S) levels in obesity and assess the relationships between DHEA-S and anthropometric, metabolic and hormonal variables. SUBJECTS AND METHODS We evaluated the serum DHEA-S levels in 217 obese but otherwise normal female subjects (age (mean ± SEM): 39.4 ± 0.9, range 18–67 years, body mass index (BMI) = 36.1 ± 0.4, range 27.1–57.1 kg/m2). RESULTS DHEA-S levels showed an age-dependent fall similar to that observed in normal women (n = 156, age 46.2 ± 1.2, range 22–69 years, BMI

To investigate the mechanism underlying the GH-releasing effect of arginine (ARG), we studied the interactions of ARG (0.5 g/kg infused i.v. over 30 min) with GHRH (1 microgram/kg i.v.) and with pyridostigmine (PD, 60 mg orally) on GH secretion in 15 children and adolescents with familial short stature (5.1-15.4 years). In a group of eight subjects ARG induced a GH increase not statistically different to that observed after GHRH (peak, mean +/- SEM: 38.0 +/- 10.4 vs 64.0 +/- 14.4 mU/l). The combined administration of ARG and GHRH led to GH levels (101 +/- 15.2 mU/l) higher than those observed after GHRH (P less than 0.025) or ARG alone (P less than 0.001) and overlapping with those recorded after combined PD and GHRH administration (111 +/- 22.4 mU/l). In the other seven subjects, ARG and PD administration induced a similar GH response either when administered alone (25.2 +/- 13.6 and 27.8 +/- 4.0 mU/l, respectively) or in combination (33.8 +/- 5.4 mU/l). In conclusion, our results show that in children ARG administration potentiates GHRH- but not PD-induced GH increase. These findings agree with the hypothesis that the GH-releasing effect of both ARG and PD is mediated via the same mechanism, namely, by suppression of endogeneous somatostatin release. Combined administration of either ARG or PD with GHRH has a similar striking GH-releasing effect which is clearly higher than that of GHRH alone.

Summary BACKGROUND AND OBJECTIVE Reduced serum levels of dehydroeplandrosterone sulphate (DHEAS) have been shown In patients with Cushing's syndrome resulting from adrenocortical adenoma, In contrast with normal DHEAS levels In patients with Cushing's disease. The elm of this study was to verify whether patients with incidentally discovered adrenocortical adenomas also have reduced levels of DHEAS. DESIGN Evaluation of serum DHEAS, serum and urinary cortisol, plasma ACTH and low dose dexamethasone suppression test In patients with adrenal Incidentaloma and Cushing's syndrome. PATIENTS Thirty-two patients with adrenal Incidentaloma and, as controls, 17 patients with overt Cushing's syndrome, were studied. RESULTS Serum DHEAS levels lower than normal were found In 21/24 (81.5 %) patients with adrenocortical Incidentaloma, but In only 1/8 patients with a mass of non-adrenocortical origin. This patient had massive bilateral metastatic infiltration of both adrenal glands and primary adrenal failure. The prevalence of low DHEAS levels in the two groups was significantly different (P= 00001). In patients with adrenocortical Incidentaloma, the prevalence of low DHEAS levels was significantly higher (P= 00001) than that found for some hormonal alterations Indicating pre-clinical hypercortlsoilsm (high urinary cortisol, unsuppressed serum cortisol after low dose dexamethasone administration and low plasma ACTH). Low DHEAS levels were found in all patients with Cushing's syndrome due to adrenocortical adenoma but in none of those with Cushing's disease. CONCLUSIONS Our results Indicate that the finding of low DHEAS levels can be considered a marker of the adrenocortical origin of an adrenal Incidentaloma, provided adrenal failure has been excluded.

To clarify the mechanism by which galanin, a 29-amino-acid peptide, increases GH secretion in man.We studied the GH-releasing effect of this neurohormone (galanin, 15 micrograms/kg) infused over 60 minutes after 120 minutes of saline, following a previous GHRH bolus (GHRH 1 microgram/kg i.v. at 0 minutes, galanin infused from 120 to 180 minutes) and coadministered with the second of two consecutive GHRH boluses (GHRH every 120 minutes, galanin infused from 120 to 180 minutes).Fourteen healthy male subjects, aged 20-34 years, in two groups (group A, 20-31 years (n = 8); group B, 25-34 years (n = 6)) were studied.Blood samples were drawn every 15 minutes of 255 minutes. Serum GH was measured in duplicate by IRMA. Statistical analysis of the data was carried out by non-parametric ANOVA test.The GH response to galanin infused 120 minutes after saline overlapped with that induced by the neuropeptide infused following previous GHRH bolus (AUC, mean +/- SEM: 317.3 +/- 73.2 vs 326.8 +/- 54.2 micrograms/l/h). The GH-releasing effect of the second GHRH bolus (126.9 +/- 32.3 micrograms/l/h) was lower than that of the first one (503.4 +/- 41.3 micrograms/l/h; P = 0.0002). Galanin markedly enhanced the GH responses to the second GHRH bolus (1118.0 +/- 212.7 micrograms/l/h; P = 0.0002 vs second GHRH bolus alone) so that it did not significantly differ from the first one (710.9 +/- 107.8 micrograms/l/h).Our results show that the GH-releasing effect of galanin is not modified by GHRH pretreatment and that the neuropeptide reinstates the GH response to the repeated GHRH stimulation in man. They suggest that these effects are due to the inhibition of hypothalamic somatostatin release.

SUMMARY There is evidence indicating that the cholinergic system positively modulates GH release probably by inhibiting somatostatinergic tone. In the present study, the effects of cholinergic enhancement by pyridostigmine, (PD), a cholin-esterases inhibitor, on GH release in normal adults (n= 14) (NA) and in both normal (n = 5) (NC) and short children (n = 19) (SC) with familial short stature (n =7) or constitutional growth delay (n= 12) were studied. In SC the insulin hypoglycaemia (IH)-induced GH increase was also studied. In both NC and SC 60 mg orally PD induced a significant GH increase with mean peak at 90 min (mean ± SEM 11.0 ± 2.2 ng/ml in NC and 11.2 ± 2.3 ng/ml in SC). The GH areas under response curve (AUC) were 379.3 ± 76.6 and 327.8 ±43.2 ng/ml/h in NC and SC respectively. In NA 120 mg orally PD induced a significant GH increase with mean peak at 120 min (5.1 ± 11 ng/ml) which was significantly lower (P < 0.05) than that observed in both NC and SC. This statistical difference was strengthened by evaluating AUC (NA: 205.6 ± 33.7 ng/ml/h, P < 0.05 vs NC and SC). The correlation of drug dosage with body area ruled out that this difference could be related to the different PD dose in adults and children. In SC, IH induced a GH increase significantly lower than that observed after PD (GH peak 7.8 ± 0.6 vs 16.4 ± 1.9 ng/ml P