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OBJECTIVE Elevated BMI, fat mass and food intake increases leptin whereas ghrelin is reduced. Ghrelin stimulates growth hormone (GH) secretion. This prospective cross-sectional study was performed to investigate the influence of GH excess on leptin and ghrelin levels at baseline and after glucose load in a large group of acromegalic patients. DESIGN/METHODS Leptin, ghrelin, GH, glucose and insulin concentrations were measured during a 3 h OGTT in 17 active, 25 inactive patients without medication (inact) and 8 inactive patients treated successfully with somatostatin analogues (inact-SA). Leptin concentration was measured using an in-house immunofluorometric assay, total serum ghrelin by a commercially available radioimmunoassay. Leptin was corrected for BMI. RESULTS During OGTT, no significant difference of baseline, nadir or AUC of leptin/BMI was seen between the groups (baseline leptin/BMI: act: 0.26 microgm(2)/lkg (0.06-0.87); inact: 0.34 microgm(2)/lkg (0.03-1.79); inact-SA: 0.29 microgm(2)/lkg (0.03-1.47). A slight but significant reduction of leptin/BMI occurred in all groups during OGTT (active p

Ghrelin is an endogenous ligand of the growth hormone (GH) secretagogue (GHS) receptor. Besides GH-releasing hormone (GHRH) and somatostatin it is thought to be a regulating factor of GH release. Ghrelin appears to be involved in sleep regulation. We showed recently that ghrelin promotes slow wave sleep and the nocturnal release of GH, cortisol and prolactin in humans. Similarly promotion of non-REM-sleep was reported in mice after systemic ghrelin. There are no data available about the pattern of ghrelin secretion during the recovery night after total sleep deprivation (TSD). Nocturnal ghrelin, GH, ACTH and cortisol plasma concentrations were determined by radioimmunoassay and simultaneously sleep EEG was recorded (23:00–07:00) during sleep before and after one night of TSD in 8 healthy subjects (3 females and 5 males, mean age 26.3yrs, SD 4.4). We observed a trend suggesting higher ghrelin secretion during the first half of the night after TSD (before TSD mean 466ng/ml, SD 113ng/ml, after TSD mean 545ng/ml, SD 176, p=0.093). In the night before TSD the maximum time of ghrelin secretion occured at 03:40 (SD 117min.) and after TSD this time point was 00:42 (SD 76min.), indicating an earlier ghrelin secretion after TSD (p

Objective: The orexigenic and adipogenic peptide hormone ghrelin is predominantly produced and secreted by the stomach and seems to transduce changes in food intake to specific neuronal circuits in the brain. The activity of ghrelin also includes stimulatory effects on the corticotropic system. However, little is known about the influence of glucocorticoids on ghrelin levels. We therefore studied human plasma ghrelin levels in the presence and absence of elevated glucocorticoid levels of either endogenous or exogenous origin. Methods: Plasma ghrelin levels were measured in five patients with chronic hypercortisolism (aged 29 – 58, median 46 years) due to Cushing’s syndrome before and after successful surgery for the adenoma, and in eight healthy controls (aged 24 – 39, median 27.5 years) before and after 30 mg prednisolone (for 5 days) once a day in the morning (median body mass index (BMI) 22.7 kg/m 2 ). Plasma ghrelin levels were measured with a commercially available radioimmunoassay. Results: In patients with Cushing’s syndrome, plasma ghrelin levels were low (median 363.2 pg/ml, range 161.9 – 525.7 pg/ml) and significantly increased by 26.6% (P ¼ 0.04) after successful surgery, while BMI decreased (median 26.2 – 24.0 kg/m 2 , P ¼ 0.04). A strong negative correlation (r ¼ 2 0.9, P ¼ 0.04) between changes in BMI and plasma ghrelin was observed. In healthy controls, plasma ghrelin levels (median 288.7 pg/ml, range 119.6 – 827.8 pg/ml) were significantly suppressed by 18.3% (P ¼ 0.04) after prednisolone treatment. Conclusions: We have shown for the first time that plasma ghrelin levels are decreased under endogenously or exogenously induced hypercortisolism, making ghrelin an unlikely candidate for causing the changes in energy balance or body composition characteristic of Cushing’s disease. However, the reduced ghrelin secretion could reflect a compensation mechanism in reaction to the metabolic consequences of chronic hypercortisolism.