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

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.

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.


Metabolism ◽  
1987 ◽  
Vol 36 (2) ◽  
pp. 105-109 ◽  
Author(s):  
A. Barbarino ◽  
L. De Marinis ◽  
A. Mancini ◽  
C. D'Amico ◽  
M. Passeri ◽  
...  

1995 ◽  
Vol 146 (2) ◽  
pp. 227-232 ◽  
Author(s):  
A Giustina ◽  
A R Bussi ◽  
R Deghenghi ◽  
B Imbimbo ◽  
M Licini ◽  
...  

Abstract The aim of our study was to investigate the effect of hexarelin, a novel GH-releasing peptide-6 analog, and GH-releasing hormone (GHRH) (alone or in combination) on GH secretion in adult patients with increased somatostatin tone due to chronic glucocorticoid excess. We studied seven adult patients undergoing long-term (no less than 6 months) immunosuppressive glucocorticoid treatment for non-endocrine diseases (six females and one male, age range 42–68 years) and one subject (female, age 31 years) with endogenous hypercortisolism due to adrenal adenoma. Six normal subjects (four females and two males) matched for sex and age with the patients and not undergoing any therapy served as controls. All the subjects underwent the following three tests in random order: (1) human GHRH (1–29)NH2 (100 μg in 1 ml saline) injected as an i.v. bolus at 0 min, (2) hexarelin (100 μg in 1 ml saline) injected as an i.v. bolus at 0 min and (3) hexarelin (100 μg in 1 ml of saline) plus GHRH (100 μg in 1 ml saline) injected as an i.v. bolus at 0 min. After GHRH alone the patients with glucocorticoid excess showed a blunted GH response as compared with normal subjects (median delta GH: 0·9, range 0–5·6 μg/l vs 7·1, range 0·3–14·9 μg/l). No significant differences were observed in the steroid-treated group with respect to normal subjects after hexarelin alone (median delta GH: 15·5, range 1·9–45·2 μg/l vs 17·9, range 5·5–53·9 μg/l). The GH responses after the combined stimuli were significantly decreased in the patients with glucocorticoid excess as compared with normal subjects (median delta GH: 43·5, range 21–56·9 μg/l vs 73·7, range 19·6-116·8 μg/l). The two stimuli acted in a synergistic fashion in both groups of subjects. It may be hypothesized that hexarelin influences the GH inhibitory effect of glucocorticoids in humans, acting at the hypothalamic somatostatin level. Journal of Endocrinology (1995) 146, 227–232


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