Effect of L-Tryptophan on Apomorphine-Induced Growth Hormone Secretion in Normal Subjects

1980 ◽  
Vol 13 (06) ◽  
pp. 331-335 ◽  
Author(s):  
S. Lal ◽  
S. Young ◽  
P. Cervantes ◽  
H. Guyda
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Normal Subjects

Role of GH in regulating nocturnal rates of lipolysis and plasma mevalonate levels in normal and diabetic humans

1992 ◽  
Vol 263 (1) ◽  
pp. E168-E172 ◽  
Author(s):  
P. J. Boyle ◽  
A. Avogaro ◽  
L. Smith ◽  
D. M. Bier ◽  
A. S. Pappu ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Fatty Acid ◽  
Cholesterol Synthesis ◽  
Gh Deficiency ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Normal Subjects ◽  
Nonesterified Fatty Acid ◽  
Rate Limiting Step ◽  
Nocturnal Increase

To define the role that nocturnal increments in growth hormone (GH) play in maintaining lipolysis, glycerol turnover was measured in six patients with GH deficiency and six normal subjects during sleep. Glycerol production initially decreased in both groups but then increased to 1.44 +/- 0.20 mumol.kg-1.min-1 by 0800 h in normal subjects, whereas GH deficiency was associated with a continuous fall to 0.77 +/- 0.10 mumol.kg-1.min-1, P less than 0.02. Nonesterified fatty acid levels paralleled these changes. Six GH-deficient patients received basal GH replacement including a pulse during sleep, which resulted in normal fasting fatty acid levels (P less than 0.05, replaced vs. chronic deficiency). To assess a possible link between the normal nocturnal increase in plasma mevalonate (the product of the rate-limiting step in cholesterol synthesis) and sleep-associated GH release, 11 GH-deficient patients and 11 normal subjects were studied. Peak nocturnal and fasting mevalonate concentrations were not correlated with GH level. We conclude that nocturnal growth hormone secretion is essential for maintaining lipolysis but that it is not related to normal increments in mevalonate and, by inference, to cholesterol synthesis during sleep

DIFFERENT EFFECTS OF EXOGENOUS CYCLIC ADENOSINE MONOPHOSPHATE AND ITS DIBUTYRYL DERIVATIVE ON PLASMA GROWTH HORMONE, GLUCOSE, INSULIN AND CORTISOL

1976 ◽  
Vol 83 (1) ◽  
pp. 15-25
Author(s):  
M. Vanderschueren-Lodeweyckx ◽  
W. Proesmans ◽  
E. Eggermont ◽  
R. Eeckels
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Normal Subjects ◽  
Immunoreactive Insulin ◽  
Plasma Growth Hormone ◽  
Hormone Levels ◽  
The Mean

ABSTRACT The effects of the infusion in four different dosages (0.001, 0.005, 0.02 and 0.2 mg/kg/min during 60 min) of cyclic 3′,5′-adenosine monophosphate and of its dibutyryl derivative on plasma growth hormone and on glucose, immunoreactive insulin and cortisol were studied in 38 normal subjects and in 10 patients with idiopathic hypopituitarism. In normal subjects cyclic 3′,5′-adenosine monophosphate provokes an increase in plasma growth hormone levels (only when a dosage of 0.2 mg/kg/min is used) without any changes in plasma glucose, insulin and cortisol. The maximal value of the means is observed 75 min after starting the infusion. Dibutyryl cyclic 3′,5′-adenosine monophosphate (0.2 and 0.02 mg/kg/min) provokes a dose-related rise in plasma growth hormone levels which is always preceded by hyperglycaemia and hyperinsulinaemia. The peak of the mean growth hormone levels occurs at 135 min after initiation of the infusion. In all but one hypopituitary patients the nucleotides do not promote growth hormone secretion. It is concluded that exogenous cyclic 3′,5′-adenosine monophosphate and its dibutyryl derivative may not be considered as analogous and that both compounds may contribute to study growth hormone release in normal subjects and in patients with growth abnormalities.

Demonstration of a role for growth hormone in glucose counterregulation

1989 ◽  
Vol 256 (6) ◽  
pp. E835-E843 ◽  
Author(s):  
P. De Feo ◽  
G. Perriello ◽  
E. Torlone ◽  
M. M. Ventura ◽  
F. Santeusanio ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Plasma Glucose ◽  
Glucose Utilization ◽  
Hepatic Glucose Production ◽  
Hormone Secretion ◽  
Plasma Catecholamines ◽  
Growth Hormone Secretion ◽  
Glucose Production ◽  
Plasma Free Fatty Acid ◽  
Normal Subjects

To test the hypothesis that growth hormone secretion plays a counterregulatory role in prolonged hypoglycemia in humans, four studies were performed in nine normal subjects. Insulin (15 mU.M-2.min-1) was infused subcutaneously (plasma insulin 27 +/- 2 microU/ml), and plasma glucose decreased from 88 +/- 2 to 53 +/- 1 mg/dl for 12 h. In study 1, plasma glucose, glucose fluxes (D-[3-3H]glucose), substrate, and counterregulatory hormone concentrations were simply monitored. In study 2 (pituitary-adrenal-pancreatic clamp), insulin and counterregulatory hormone secretions (except for catecholamines) were prevented by somatostatin (0.5 mg/h iv) and metyrapone (0.5 g/4 h po), and glucagon, cortisol, and growth hormone were reinfused to reproduce the concentrations of study 1. In study 3 (lack of growth hormone increase), the pituitary-adrenal-pancreatic clamp was performed with maintenance of plasma growth hormone at basal levels, and glucose was infused whenever needed to reproduce plasma glucose concentration of study 2. Study 4 was identical to study 3, but exogenous glucose was not infused. Isolated lack of a growth hormone response caused a decrease in hepatic glucose production and an increase in glucose utilization that resulted in an approximately 25% greater hypoglycemia despite compensatory increases in plasma catecholamines. Plasma free fatty acid, 3-beta-hydroxybutyrate, and glycerol concentrations were reduced approximately 50%. It is concluded that growth hormone normally plays an important counterregulatory role during hypoglycemia by augmenting glucose production, decreasing glucose utilization, and accelerating lipolysis.

Galanin does not affect the growth hormone-releasing hormone-stimulated growth hormone secretion in patients with hyperthyroidism

1992 ◽  
Vol 127 (6) ◽  
pp. 504-508 ◽  
Author(s):  
Andrea Giustina ◽  
Anna Rosa Bussi ◽  
Fabio Legati ◽  
Simonetta Bossoni ◽  
Massimo Licini ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Random Order ◽  
Normal Subjects ◽  
Graves Disease ◽  
Growth Hormone Releasing Hormone ◽  
Gh Secretion ◽  
Hyperthyroid Patients ◽  
Secretory Capacity

Patients with hyperthyroidism have reduced spontaneous and stimulated growth hormone (GH) secretion. The aim of our study was to evaluate the effects of galanin, a novel neuropeptide which stimulates GH secretion in man, on the GH response to GHRH in patients with hyperthyroidism. Eight untreated hyperthyroid patients with Graves' disease (6F, 2M, aged 25–50 years) and six healthy volunteers (3F, 3M, aged 27–76 years) underwent from - 10 to 30 min in random order: (i) porcine galanin, iv, 500 μg in 100 ml saline; or (ii) saline, iv, 100 ml. A bolus of human GHRH(1-29)NH2, 100 μg, was injected iv at 0 min. Hyperthyroid patients showed blunted GH peaks after GHRH+saline (10.2±2.5 μg/l) compared to normal subjects (20.7±4.8 μg/l, p< 0.05). GH peaks after GHRH+ galanin were also significantly lower in hyperthyroid subjects (12.5±3 μg/l) compared to normal subjects (43.8±6 μg/l, p<0.05). That galanin is not able to reverse the blunted GH response to GHRH in hyperthyroidism suggests that hyperthyroxinemia may either increase the somatostatin release by the hypothalamus or directly affect the pituitary GH secretory capacity.

scholarly journals The dopaminergic regulation of plasma growth hormone secretion in normal subjects.

1986 ◽  
Vol 148 (2) ◽  
pp. 151-158 ◽  
Author(s):  
KUNIHIKO HANEW ◽  
SHUICHI SATO ◽  
ATSUSHI SASAKI ◽  
MEIGAN GOH ◽  
YASUYUKI SHIMIZU ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Normal Subjects ◽  
Plasma Growth Hormone ◽  
Dopaminergic Regulation

Dissociation between circulating concentrations of immunoreactive growth hormone releasing factor and growth hormone in normal human subjects

1987 ◽  
Vol 72 (2) ◽  
pp. 181-185 ◽  
Author(s):  
A. M. Sopwith ◽  
Elizabeth S. Penny ◽  
N. Lytras ◽  
G. M. Besser ◽  
Lesley H. Rees
Keyword(s):  
Growth Hormone ◽  
Human Growth Hormone ◽  
Human Subjects ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Human Growth ◽  
Normal Subjects ◽  
Peripheral Circulation ◽  
Growth Hormone Releasing Factor ◽  
Specific Radioimmunoassay

1. Using a highly specific radioimmunoassay we have measured immunoreactive human growth hormone releasing factor (ir-hGRF) concentrations in the peripheral circulation of a total of 12 normal subjects. 2. Neither insulin-induced hypoglycaemia, intravenous arginine nor oral carbohydrate caused any change in venous plasma ir-hGRF concentrations, despite the expected stimulation and suppression respectively of growth hormone secretion. 3. Growth hormone secretion was not increased by oral fat or protein but each of these two foods stimulated ir-hGRF concentrations two- to fourfold. 4. Spontaneous pulses of growth hormone secretion on control days were unaccompanied by any increase in plasma ir-hGRF. 5. The dissociation between peripheral circulating ir-hGRF and growth hormone responses demonstrated under different circumstances suggests that an important source of human growth hormone releasing factor lies outside the hypothalamus and that secretion from this source is unconnected with the normal control of pituitary growth hormone secretion.

EFFECT OF AMINOPHYLLINE ON GROWTH HORMONE SECRETION IN MAN

1974 ◽  
Vol 76 (3) ◽  
pp. 488-494 ◽  
Author(s):  
M. Peracchi ◽  
F. Cavagnini ◽  
A. E. Pontiroli ◽  
U. Raggi ◽  
A. Malinverni ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Blood Glucose ◽  
Intravenous Infusion ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Normal Subjects ◽  
Gh Secretion ◽  
Inhibiting Effect ◽  
Plasma Ffa ◽  
Serum Gh

ABSTRACT The effects of intravenously administered aminophylline on growth hormone (GH) secretion have been studied in sixteen normal subjects and four acromegalic patients. Intravenous infusion of theophylline ethylenediamine 480 mg over a 30 min period did not alter the blood glucose and serum GH levels in six normal subjects but raised the plasma FFA by 88 %. By contrast, in four acromegalic patients theophylline administration resulted in a fall of the serum GH levels by 17.6–51.7 %, mean 36.5%. In ten normal subjects the infusion of the drug clearly blunted the GH response to insulin hypoglycaemia without modifying the decrease in blood glucose and plasma FFA induced by insulin: mean peak GH values decreased from 32.7 ± 3.39 to 21.4 ± 4.10 ng/ml (P < 0.025). These data seem to indicate that theophylline has an overall inhibiting effect on the hypothalamic-hypophyseal axis for GH secretion.

INTERACTION BETWEEN THYROTROPHIN, CORTICOTROPHIN AND GROWTH HORMONE SECRETION IN MAN

1971 ◽  
Vol 51 (4) ◽  
pp. 699-706 ◽  
Author(s):  
G. M. BESSER ◽  
J. G. RATCLIFFE ◽  
J. R. KILBORN ◽  
B. J. ORMSTON ◽  
R. HALL
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Normal Subjects ◽  
Acth Secretion ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Dexamethasone Suppression ◽  
Control Injection

SUMMARY Thyrotrophin (TSH) release in response to intravenous synthetic thyrotrophin releasing hormone (TRH) was unaltered by simultaneous corticotrophin (ACTH) and growth hormone secretion induced by hypoglycaemia or methylamphetamine in normal subjects. Secretion of growth hormone was the same whether or not TSH was secreted. While the increments in plasma corticosteroids and ACTH after methylamphetamine administration were not different whether TRH or a control injection was given, they rose more during insulin-induced hypoglycaemia when TRH was given as well. This could have been due to a slightly greater degree of stress after TRH + insulin than insulin alone. Overnight dexamethasone suppression of basal ACTH secretion did not alter the TSH response to TRH. Unlike the rat, there is no evidence suggesting competition between pituitary mechanisms involved in ACTH, growth hormone and TSH release in man.

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