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 Molecular evolution of the growth hormone-releasing hormone/pituitary adenylate cyclase-activating polypeptide gene family. Functional implication in the regulation of growth hormone secretion

2000 ◽  
Vol 25 (2) ◽  
pp. 157-168 ◽  
Author(s):  
M Montero ◽  
L Yon ◽  
S Kikuyama ◽  
S Dufour ◽  
H Vaudry
Keyword(s):  
Growth Hormone ◽  
Molecular Evolution ◽  
Adenylate Cyclase ◽  
Gene Family ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Pituitary Adenylate Cyclase

Growth hormone-releasing hormone (GHRH) and pituitary adenylate cyclase-activating polypeptide (PACAP) belong to the same superfamily of regulatory neuropeptides and have both been characterized on the basis of their hypophysiotropic activities. This review describes the molecular evolution of the GHRH/PACAP gene family from urochordates to mammals and presents the hypothesis that the respective roles of GHRH and PACAP in the control of GH secretion are totally inverted in phylogenetically distant groups of vertebrates. In mammals, GHRH and PACAP originate from distinct precursors whereas, in all submammalian taxa investigated so far, including birds, amphibians and fish, a single precursor encompasses a GHRH-like peptide and PACAP. In mammals, GHRH-containing neurons are confined to the infundibular and dorsomedial nuclei of the hypothalamus while PACAP-producing neurons are widely distributed in hypothalamic and extrahypothalamic areas. In fish, both GHRH- and PACAP-immunoreactive neurons are restricted to the diencephalon and directly innervate the adenohypophysis. In mammals and birds, GHRH plays a predominant role in the control of GH secretion. In amphibians, both GHRH and PACAP are potent stimulators of GH release. In fish, PACAP strongly activates GH release whereas GHRH has little or no effect on GH secretion. The GHRH/PACAP family of peptides thus provides a unique model in which to investigate the structural and functional facets of evolution.

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.

Sex-related naloxone influence on growth hormone-releasing hormone-induced growth hormone secretion in normal subjects

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

EFFECT OF l-DOPA ADMINISTRATION ON GROWTH HORMONE SECRETION IN NORMAL SUBJECTS AND PARKINSONIAN PATIENTS

1972 ◽  
Vol 54 (3) ◽  
pp. 425-433 ◽  
Author(s):  
F. CAVAGNINI ◽  
M. PERACCHI ◽  
G. SCOTTI ◽  
U. RAGGI ◽  
A. E. PONTIROLI ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Normal Subjects ◽  
Significant Rise ◽  
Arginine Infusion ◽  
Physiological Regulation ◽  
Gh Secretion ◽  
Before And After ◽  
Serum Gh

SUMMARY The effect of both oral and intravenous administration of l-DOPA on growth hormone (GH) secretion was studied in a group of normal volunteers: a significant rise of serum GH levels was observed in both cases. Growth hormone release in response to insulin hypoglycaemia and to arginine infusion was evaluated in a group of Parkinsonian patients before and after 25 days' treatment with l-DOPA plus a DOPA-decarboxylase inhibitor. In addition, GH response to the above stimuli was studied in a group of patients who had been under treatment for more than 6 months with l-DOPA alone. In untreated Parkinsonian patients, GH response to insulin hypoglycaemia was at the lower limit of normal range while arginine-induced GH release was significantly reduced. Treatment with l-DOPA did not increase GH responses. Some possible interpretations of the results are discussed. The findings support the possibility that dopamine plays a role in the physiological regulation of GH secretion, as in the case of luteinizing hormone, follicle-stimulating hormone and prolactin release.

Comparison of the effects of growth hormone-releasing hormone and hexarelin, a novel growth hormone-releasing peptide-6 analog, on growth hormone secretion in humans with or without glucocorticoid excess

1995 ◽  
Vol 146 (2) ◽  
pp. 227-232 ◽  
Author(s):  
A Giustina ◽  
A R Bussi ◽  
R Deghenghi ◽  
B Imbimbo ◽  
M Licini ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Adrenal Adenoma ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Random Order ◽  
Normal Subjects ◽  
Treated Group ◽  
Adult Patients ◽  
Glucocorticoid Treatment ◽  
Releasing Hormone

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

scholarly journals Intravenous administration of ghrelin stimulates growth hormone secretion in vagotomized patients as well as normal subjects

2004 ◽  
pp. 447-450 ◽  
Author(s):  
R Takeno ◽  
Y Okimura ◽  
G Iguchi ◽  
M Kishimoto ◽  
T Kudo ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Direct Action ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Normal Subjects ◽  
Vagal Nerve ◽  
Gh Secretion ◽  
Afferent Vagal ◽  
Vagal Afferent ◽  
Plasma Gh

OBJECTIVE: Ghrelin is a potent peptide stimulating GH secretion. Besides its direct action on the pituitary, ghrelin has been reported to stimulate GH release via the vagal afferent nerve in rats. To examine the involvement of vagal nerve in ghrelin-induced GH secretion in humans, GH responses to ghrelin were compared between vagotomized patients with gastrectomy and normal subjects. METHODS: Ghrelin (0.2 microg/kg) or GHRH (1 microg/kg) was administered intravenously in vagotomized patients and normal subjects on separate days, and plasma GH responses to the stimuli were examined. RESULTS: Ghrelin caused a significant plasma GH rise in both vagotomized patients and normal subjects. Peak GH levels in vagotomized patients (37.5+/-16.9 ng/ml) were not different from those in normal subjects (29.9+/-23.1 ng/ml). The areas under the curve of GH response to ghrelin did not differ between the two groups. GHRH also increased GH levels, and peak GH levels and areas under the curve after GHRH stimulation were also comparable between vagotomized patients and normal subjects. CONCLUSIONS: In the present study, the involvement of the afferent vagal nerve in ghrelin-induced GH secretion was not confirmed in humans.

Pyridostigmine enhances, but does not normalise, the GH response to GH-releasing hormone in obese subjects

1990 ◽  
Vol 122 (3) ◽  
pp. 385-390 ◽  
Author(s):  
R. C. Castro ◽  
J. G. H. Vieira ◽  
A. R. Chacra ◽  
G. M. Besser ◽  
A. B. Grossman ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Acetylcholinesterase Inhibitor ◽  
Random Order ◽  
Normal Subjects ◽  
Obese Patients ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Obese Subjects ◽  
Higher Doses ◽  
Hormone Responsiveness

Abstract Obese patients are characterised by several neuroendocrine abnormalities, including characteristically a decrease in growth hormone responsiveness to GH-releasing hormone. In normal subjects, the GH response to GHRH is enhanced by the acetylcholinesterase inhibitor, pyridostigmine. We have studied the effect of this drug on GH secretion in gross obesity. Twelve obese patients were studied (mean weight 156% of ideal) and compared with a group of 8 normal volunteers. Each subject was initially studied on two occasions, in random order, with GHRH (1–29) NH2 100 μg iv alone and following pretreatment with pyridostigmine 120 mg orally one hour prior to GHRH. In obese patients, the GH response to GHRH was significantly blunted when compared to controls (GH peak: 20 ± 4 vs 44 ± 16 μg/l; mean ± sem). After pyridostigmine, the response to GHRH was enhanced in the obese subjects, but remained significantly reduced compared to non-obese subjects treated with GHRH and pyridostigmine (GH peak: 30 ± 5 vs 77 ± 20 μg/l, respectively). In 6 subjects, higher doses of GHRH or pyridostigmine did not further increase GH responsiveness in obese patients. Our results suggest that obese patients have a disturbed cholinergic control of GH release, probably resulting from increased somatostatinergic tone. This disturbed regulation may be responsible, at least in part, for the blunted GH responses to provocative stimuli.

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