Effect of sleep deprivation on the growth hormone response to the alpha-2 adrenergic receptor agonist, clonidine, in normal subjects

1997 ◽  
Vol 104 (2-3) ◽  
pp. 291-298 ◽  
Author(s):  
S. Lal ◽  
J. X. Thavundayil ◽  
B. Krishnan ◽  
N. P. V. Nair ◽  
G. Schwartz ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Sleep Deprivation ◽  
Adrenergic Receptor ◽  
Receptor Agonist ◽  
Normal Subjects ◽  
Growth Hormone Response ◽  
Hormone Response ◽  
Adrenergic Receptor Agonist

Effects of Desipramine Treatment upon Central Adrenoceptor Function in Normal Subjects

1984 ◽  
Vol 145 (2) ◽  
pp. 139-145 ◽  
Author(s):  
T. H. Corn ◽  
C. Thompson ◽  
S. A. Checkley
Keyword(s):  
Growth Hormone ◽  
Time Course ◽  
Normal Subjects ◽  
Growth Hormone Response ◽  
Hormone Response ◽  
Acute Effects ◽  
Down Regulation ◽  
Adaptive Changes ◽  
Stopping Treatment ◽  
Rebound Increase

SummarySix normal subjects were given clonidine infusions after 0, 1 and 3 weeks of treatment with desipramine (2 mg/kgm) and at 1 and 3 weeks after withdrawal from desipramine. The sedative and hypotensive effects of clonidine were inhibited after one and three weeks of desipramine treatment, and returned to normal after stopping treatment without any rebound increase. Such a time-course can be explained in terms of the acute effects of the drug, no adaptive changes at receptors need be invoked.By contrast, the growth hormone response to clonidine tended to be increased after one week of desipramine, reduced after three weeks of treatment, and further reduced after discontinuation. Such a time-course is consistent with an adaptive down regulation at α2 adrenoceptors in response to their acute stimulation, due to noradrenaline re-uptake blockade.

Growth hormone response to clonidine in male patients with panic disorder untreated by antidepressants

1992 ◽  
Vol 22 (4) ◽  
pp. 1059-1062 ◽  
Author(s):  
M. Schittecatte ◽  
M. Ansseau ◽  
G. Charles ◽  
R. Machowski ◽  
P. papart ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Panic Disorder ◽  
Adrenergic Receptor ◽  
Antidepressant Therapy ◽  
Growth Hormone Response ◽  
Hormone Response ◽  
Receptor Sensitivity ◽  
Male Patients

SynopsisWe report a non-significantly higher growth hormone (GH) response to intravenous clonidine administration (150 μg) in 10 male patients with panic disorder who had never received antidepressant therapy than in 10 matched controls. These results are consistent with data suggesting a normal or increased adrenergic receptor sensitivity in panic disorder patients.

The Effect of Hypoglycaemia on Oral Glucose Tolerance in Normal Subjects and Patients with Pituitary and Adrenal Disorders

1970 ◽  
Vol 39 (5) ◽  
pp. 663-674 ◽  
Author(s):  
N. W. Oakley ◽  
H. S. Jacobs ◽  
R. C. Turner ◽  
J. Williams ◽  
C. Dos ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Glucose Tolerance ◽  
Normal Subjects ◽  
Growth Hormone Response ◽  
Saline Control ◽  
Oral Glucose ◽  
Hormone Response ◽  
Oral Glucose Tolerance ◽  
Brittle Diabetes ◽  
Insulin Test

1. Hypoglycaemia induces glucose intolerance in normal subjects—the ‘Somogyi effect’–and may be responsible for some instances of ‘brittle diabetes’. This effect may be mediated through the growth hormone response to hypoglycaemia, but other possible hormonal mechanisms have not been excluded. 2. Paired 2-h oral glucose tolerance tests have been carried out 2 h after both (a) i.v. saline (control day) and (b) i.v. insulin (test day) in four normal subjects and twenty-seven patients with pituitary and adrenal under- and over-activity. Plasma glucose, insulin, Cortisol and growth hormone have been estimated at half-hourly intervals during the 4 h of each study. 3. A significant Somogyi effect is usually seen only when there is a growth hormone response to insulin-induced hypoglycaemia; hypopituitary subjects do not show the effect. 4. There is a correlation between the extent of the Somogyi effect and the growth hormone response to insulin, using a simple derived index to represent each function (P < 0·05). 5. Insulin secretion in normal subjects tends to be higher on the test than the control day, making inhibition of insulin release an unlikely primary mechanism. 6. The presence or absence of a Somogyi effect could not be related to insulin-induced changes in plasma Cortisol values. 7. Examination of individual cases supports the view that, while growth hormone may be mainly reponsible for the Somogyi effect, yet it is sometimes difficult to explain the effect without invoking other endocrine mechanisms.

Growth Hormone and other Responses to Clonidine in Patients with Endogenous Depression

1981 ◽  
Vol 138 (1) ◽  
pp. 51-55 ◽  
Author(s):  
S. A. Checkley ◽  
A. P. Slade ◽  
E. Shur
Keyword(s):  
Growth Hormone ◽  
Normal Subjects ◽  
Endogenous Depression ◽  
Growth Hormone Response ◽  
Hormone Response ◽  
Sedative Effects ◽  
Drug Free ◽  
Age And Sex ◽  
Neuroendocrine Systems

SummaryThe growth hormone response to clonidine was significantly less in 10 drug-free patients with endogenous depression than in 10 normal subjects who were individually matched with the patients for age and sex. The hypotensive and sedative effects of clonidine in the two groups were similar. The findings may indicate a defect at central a adrenoceptors at least in neuroendocrine systems.

Lack of growth hormone response to acute administration of dexamethasone in anorexia nervosa

1995 ◽  
Vol 132 (2) ◽  
pp. 152-158 ◽  
Author(s):  
Massimo Scacchi ◽  
Cecilia Invitti ◽  
Angela I Pincelli ◽  
Claudio Pandolfi ◽  
Antonella Dubini ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Anorexia Nervosa ◽  
Normal Subjects ◽  
High Plasma ◽  
Normal Weight ◽  
Growth Hormone Response ◽  
Acute Administration ◽  
Hormone Response ◽  
Gh Secretion ◽  
Plasma Gh

Scacchi M, Invitti C, Pincelli AI, Pandolfi C, Dubini A, Cavagnini F. Lack of growth hormone response to acute administration of dexamethasone in anorexia nervosa. Eur J Endocrinol 1995;132:152–8. ISSN 0804–4643 High plasma growth hormone (GH) levels, associated with abnormal hormone responses to provocative stimuli, point to an altered GH secretion in anorexia nervosa. The GH-releasing effect of acutely administered glucocorticoids, firmly established in normal subjects, has not been reported in these patients. In this study, acute iv administration of 4 mg of dexamethasone, compared with saline, increased plasma GH in nine normal-weight women (AUC 848.2 ± 127.95 vs 242.8 ± 55.35 μg·l−1·min−1, p < 0.05, respectively) but was ineffective in 11 anorectic patients (AUC 3271.8 ± 1407.11 vs 2780.0 ± 1162.04 μg·l−1·min−1, NS). After dexamethasone, a significant lowering of plasma cortisol was observed in normal women (AUC 25367.0 ± 3128.43 vs 47347.1 ± 4456.61 nmol·l−1·min−1, after dexamethasone and saline, respectively, p < 0.05), but not in anorectic patients (AUC 77809.3 ± 8499.92 vs 78454.9 ± 7603.62 nmol·l−1·min−1, NS). In both groups, plasma adrenocorticotrophin (ACTH) displayed a significant decrease after dexamethasone (AUC 523.6 ± 92.08 vs 874.2 ± 115.03 pmol·l−1·min−1, p < 0.05, after dexamethasone and saline, respectively, in anorectic patients and 377.5 ± 38.41 vs 1004.9 ± 200.51 pmol·l−1·min−1, p < 0.05, in controls). However, when considering the hormonal decremental areas, a significant dexamethasone-induced ACTH inhibition, compared to saline, was evidenced in normal (ΔAUC –414.4 ± 65.75 vs 222.9 ± 42.40 pmol·l−1·min−1, p < 0.05) but not in anorectic women (ΔAUC –254.2 ± 96.92 vs 2.9 ± 132.32 pmol·l−1·min−1, NS). In conclusion, compared to normal subjects, anorectic patients do not display an increase of plasma GH levels and show a lower degree of inhibition of the hypothalamic–pituitary–adrenal axis following acute iv administration of dexamethasone. This observation broadens the array of the abnormal GH responses to provocative stimuli in anorexia nervosa and supports the existence, in these patients, of a decreased hypothalamic somatostatin secretion, although the possibility of a reduced tissue sensitivity to glucocorticoids cannot be excluded. Francesco Cavagnini, 2nd Chair of Endocrinology, University of Milan, Istituto Scientifico Ospedale San Luca, Centro Auxologico Italiano, via Spagnoletto 3, 20149 Milano, Italy

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