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 ◽  
...  
1976 ◽  
Vol 83 (1) ◽  
pp. 15-25
Author(s):  
M. Vanderschueren-Lodeweyckx ◽  
W. Proesmans ◽  
E. Eggermont ◽  
R. Eeckels

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.


1992 ◽  
Vol 263 (1) ◽  
pp. E168-E172 ◽  
Author(s):  
P. J. Boyle ◽  
A. Avogaro ◽  
L. Smith ◽  
D. M. Bier ◽  
A. S. Pappu ◽  
...  

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


1980 ◽  
Vol 13 (06) ◽  
pp. 331-335 ◽  
Author(s):  
S. Lal ◽  
S. Young ◽  
P. Cervantes ◽  
H. Guyda

1976 ◽  
Vol 50 (4) ◽  
pp. 241-247 ◽  
Author(s):  
J. R. Sutton ◽  
N. L. Jones ◽  
C. J. Toews

1. Seven healthy males were studied during cycle ergometer exercise at 33%, 66% and 90% of V̇o2 max. on three occasions when NH4Cl, NaHCO3 or CaCO3 (as a control substance) were administered in gelatin capsules double blind and in randomized order. Plasma growth hormone (HGH), lactic acid and hydrogen ion concentration ([H+])weremeasured at frequent intervals. 2. Ammonium chloride produced highest blood [H+] and NaHCO3 the lowest. These differences were maintained during exercise and in recovery. Plasma lactic acid concentrations were similar at rest. At 66%, 90% V̇o2 max. and recovery lactic acid was highest with NaHCO3 and lowest with NH4Cl. 3. Exercise stimulated HGH secretion in all studies and the elevation was proportional to the intensity of the exercise. NH4Cl caused a variable elevation of HGH at rest and 33% V̇o2 max. At 66% V̇o2 max., plasma HGH was significantly elevated to similar concentrations in all studies and, at 90% V̇o2 max., HGH was highest with NaHCO3. 4. An infusion of sodium l(+)-lactate producing plasma lactate concentrations of 3–5 mmol/l did not influence HGH secretion. 5. Exercise is a physiological stimulus to HGH secretion and the mechanism is independent of blood [H+] and lactate concentrations.


1992 ◽  
Vol 127 (5) ◽  
pp. 416-419 ◽  
Author(s):  
Koji Nakagawa ◽  
Tatsuya Ishizuka ◽  
Chikara Shimizu ◽  
Yoshito Ito ◽  
Ichiji Wakabayashi

There is increasing evidence to suggest that supraphysiological doses of glucocorticoids suppress growth hormone secretion in vivo by augmenting somatostatin release from the hypothalamus; previously, we reported an increase in hypothalamic somatostatin content in dexamethasone-treated rats. To further examine whether the production of somatostatin really is augmented, hypothalamic somatostatin mRNA levels were determined by the Northern blot technique in female rats receiving 330 μg of dexamethasone daily for three days. In two series of experiments, hypothalamic somatostatin mRNA levels in dexamethasone-treated rats were significantly (p<0.05) increased to 133±19 (mean±sd)% and 153±38% of the controls. In the dexamethasone-treated rats, plasma growth hormone levels were markedly suppressed compared with those of the controls. These results further support the hypothesis that pharmacological doses of glucocorticoids increase the production and release of somatostatin from the hypothalamus and thus inhibit growth hormone secretion, overriding the direct stimulatory effect of glucocorticoids on growth hormone production at the pituitary level.


1981 ◽  
Vol 97 (4) ◽  
pp. 448-453 ◽  
Author(s):  
C. G. Scanes ◽  
S. Harvey ◽  
B. A. Morgan ◽  
M. Hayes

Abstract. Variations in plasma growth hormone (GH) concentrations following iv or sc administration of synthetic thyrotrophin-releasing hormone (TRH, Pyr-His-Pro-NH2) have been followed in immature and adult domestic fowl. TRH markedly stimulated GH secretion in newly hatched (1 and 2 day old) chicks and in 6-week-old cockerels but in adult male or female birds of two strains had very little effect, if any. Intravenous injection of 4 TRH analogues (Pyr-His-Mep-NH2, Pyr-Meh-Mep-NH2, Pyr-Meh-Mep-NH and Pyr-Meh-Pro-NH2) were also potent GH secretagogues in 6-week-old birds. The stimulatory effect of TRH or the TRH-analogues on GH secretion was not dose-related.


1989 ◽  
Vol 256 (6) ◽  
pp. E835-E843 ◽  
Author(s):  
P. De Feo ◽  
G. Perriello ◽  
E. Torlone ◽  
M. M. Ventura ◽  
F. Santeusanio ◽  
...  

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.


1971 ◽  
Vol 66 (4) ◽  
pp. 577-586 ◽  
Author(s):  
R. C. Turner ◽  
B. Schneeloch ◽  
P. Paterson

ABSTRACT Plasma immunoreactive insulin and growth hormone of 20–24 weeks' gestation human foetuses were assayed in serial samples following delivery by hysterotomy. The mean umbilical cord plasma growth hormone concentration was 71 ng/ml (range 13–120 ng/ml) and the mean plasma insulin was 5 μU/ml (range 2–8 μU/ml). Following delivery the growth hormone levels increased, but there was no significant change in plasma insulin concentration. The hypothalamic-hypophyseal axis controlling growth hormone secretion appears to be developed by 20 weeks' gestation, and »stress« appears to be a provocative stimulus.


1992 ◽  
Vol 127 (6) ◽  
pp. 504-508 ◽  
Author(s):  
Andrea Giustina ◽  
Anna Rosa Bussi ◽  
Fabio Legati ◽  
Simonetta Bossoni ◽  
Massimo Licini ◽  
...  

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.


Sign in / Sign up

Export Citation Format

Share Document