Growth hormone (GH) secretion in active acromegaly after the combined administration of GH-releasing hormone and GH-releasing peptide-6

1994 ◽  
Vol 79 (2) ◽  
pp. 456-460 ◽  
Author(s):  
V. Popovic
Keyword(s):  
Growth Hormone ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Combined Administration ◽  
Active Acromegaly

Growth hormone (GH) responses to the combined administration of GH-releasing hormone plus GH-releasing peptide 6 in adults with GH deficiency

1995 ◽  
Vol 132 (6) ◽  
pp. 712-715 ◽  
Author(s):  
A Leal-Cerro ◽  
E Garcia ◽  
R Astorga ◽  
FF Casanueva ◽  
C Dieguez
Keyword(s):  
Growth Hormone ◽  
Gh Deficiency ◽  
Hormone Deficiency ◽  
Santiago De Compostela ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Factor I ◽  
Gh Replacement ◽  
Combined Administration ◽  
Plasma Gh

Leal-Cerro A, Garcia E, Astorga R, Casanueva FF, Dieguez C. Growth hormone (GH) responses to the combined administration of GH-releasing hormone plus GH-releasing peptide 6 in adults with GH deficiency. Eur J Endocrinol 1995;132:712–5. ISSN 0804–4643 In recent years the health problems of adults with growth hormone deficiency (GHD) and the benefits of GH replacement therapy have received considerable attention. However, the reliability of conventional GH tests in the assessment of pituitary GH reserve in this group of patients is still controversial. In this study, we assessed GH secretion after the combined administration of GH-releasing hormone (GHRH) (1 μg/kg iv) and GH-releasing peptide 6 (GHRP-6, 1 μg/kg iv) in adult patients diagnosed with GHD by conventional GH testing, and correlate this response with insulin-like growth factor I levels. Twenty-one subjects (13 male, 8 female) with long-standing diagnosis of GHD aged 21–54 years were studied. In 13 subjects GH responses to GHRH plus GHRP-6 were markedly reduced (peak GH response <10 mU/I), whereas in the remaining eight the response was greater (range 11–100 mU/l), In conclusion, our data show that combined administration of GHRH plus GHRP-6 elicited a significant increase in plasma GH levels in about 40% of patients diagnosed with GHD by conventional GH testing. C Dieguez, PO Box 563, 15700 Santiago de Compostela, Spain

Failure to confirm a growth hormone-releasing activity of corticotropin-releasing hormone in acromegaly: Comparison with the effects of other hypothalamic hormones

1991 ◽  
Vol 125 (5) ◽  
pp. 487-490 ◽  
Author(s):  
Hajime Watanobe ◽  
Shinsuke Sasaki ◽  
Kazuo Takebe
Keyword(s):  
Growth Hormone ◽  
Vasoactive Intestinal Peptide ◽  
Corticotropin Releasing Hormone ◽  
Negative Data ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Hypothalamic Hormones ◽  
Active Acromegaly ◽  
Plasma Gh

Abstract. We re-examined whether CRH stimulates GH secretion in acromegaly. Human CRH (100 μg) was given as an iv bolus to 15 patients with active acromegaly, and plasma GH levels were measured before and at intervals up to 120 min after the injection. For comparison, we assessed in all the patients the effects of TRH (500 μg), GnRH (100 μg), vasoactive intestinal peptide (100 μg) and peptide histidine methionine (100 μg), which are known paradoxically to stimulate GH secretion in acromegaly. A paradoxical GH response (>50% above the basal) to TRH, GnRH, vasoactive intestinal peptide and peptide histidine methionine was observed in 12 (80%), 4 (27%), 5 (33%) and 2 (13%) patients, respectively. All the patients were responsive to at least one of these 4 peptides. However, none of the patients showed a positive GH response to hCRH. These results do not support a GH-releasing activity of CRH in acromegaly. Even if CRH has such an effect, it does not appear as potent as TRH, GnRH, vasoactive intestinal peptide and peptide histidine methionine. However, the possibility cannot be excluded that our negative data might have been due to the use of hCRH vs ovine CRH in earlier studies.

Influence of endogenous cholinergic tone and α-adrenergic pathways on growth hormone responses to His-d-Trp-Ala-Trp-d-Phe-Lys-NH2 in the dog

1993 ◽  
Vol 138 (2) ◽  
pp. 211-218 ◽  
Author(s):  
J. Muruais ◽  
A. Peñalva ◽  
C. Dieguez ◽  
F. F. Casanueva
Keyword(s):  
Growth Hormone ◽  
Inhibitory Effect ◽  
Adrenergic Agonist ◽  
Stimulatory Action ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Combined Administration ◽  
Cholinergic Tone ◽  
Basal Plasma ◽  
Plasma Gh

ABSTRACT His-d-Trp-Ala-Trp-d-Phe-Lys-NH2 (GHRP-6) is a synthetic peptide unrelated to any known hypothalamic-releasing hormone including growth hormone-releasing hormone (GHRH). Interestingly, this peptide induces a dose-related increase in plasma GH levels in all species tested so far. The aim of this study was to investigate the action of GHRP-6 alone or in combination with GHRH on GH release in dogs. In addition, the activation or blockade of endogenous cholinergic tone and α-1 adrenoceptors on GHRP-6-stimulated GH secretion was assessed. In adult Beagle dogs (n = 10), GHRP-6 (90 μg i.v.) increased basal GH levels from 2·6 ± 1·5 to 14·4 ± 3·1 μg/l (mean ± s.e.m.) after 15 min. GHRH (50 μg i.v.) induced a GH peak of 9·7 ± 2·2 μg/l at 15 min. The combined administration of GHRP-6 and GHRH strikingly potentiated canine GH release with a peak of 54 ± 9·0 μg/l (P <0·01). Pretreatment with the cholinergic agonist pyridostigmine (30 mg per os) increased GHRP-6-stimulated GH secretion (37·9 ± 10·1 μg/l P <0·05), while the muscarinic blocker atropine (100 μg i.v.) completely abolished (GH peak lower than 2 μg/l) the stimulatory action of GHRP-6. On the other hand, administration of the α-2 adrenergic agonist clonidine (4 pg/kg i.v.) increased basal plasma GH levels without affecting GH responses to GHRP-6. Finally, while the α-1 adrenergic agonist methoxamine (5 mg i.v.) did not significantly increase GH responses to GHRP-6, administration of the α-1 adrenoceptor antagonist prazosin (20 mg i.v.) reduced GHRP-6-induced GH secretion (area under curve, 206 ± 39 vs 557 ± 172, P <0·05). In summary, the synergistic effect of the combined administration of maximal doses of GHRP-6 and GHRH suggests that these two peptides act through different mechanisms. The finding that cholinergic drugs were able to modulate the GH secretion elicited by GHRP-6 argues against the hypothesis that such a peptide acts by influencing hypothalamic somatostatin release and suggests that it acts directly at the pituitary level. Finally, the unexpected lack of effect of clonidine and the inhibitory effect of prazosin on GHRP-6-induced GH secretion suggests that the role of α-adrenergic pathways in GH secretion is more complex than previously thought. Journal of Endocrinology (1993) 138, 211–218

scholarly journals Growth Hormone-Releasing Peptide-2 Stimulates GH Secretion in GH-Deficient Patients with Mutated GH-Releasing Hormone Receptor1

2001 ◽  
Vol 86 (7) ◽  
pp. 3279-3283
Author(s):  
Rogério G. Gondo ◽  
Manuel H. Aguiar-Oliveira ◽  
César Y. Hayashida ◽  
Sergio P. A. Toledo ◽  
Neusa Abelin ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Releasing Hormone ◽  
Gh Secretion

scholarly journals From growth hormone-releasing peptides to ghrelin: discovery of new modulators of GH secretion

2006 ◽  
Vol 50 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Ana Maria J. Lengyel
Keyword(s):  
Growth Hormone ◽  
Protein Kinase ◽  
C Protein ◽  
Releasing Hormone ◽  
Gh Secretagogues ◽  
Main Site ◽  
Gh Secretion ◽  
Kinase C ◽  
Growth Hormone Releasing Peptides

Growth hormone (GH)-releasing hormone and somatostatin modulate GH secretion. A third mechanism has been discovered in the last decade, involving the action of GH secretagogues. Ghrelin is a new acylated peptide produced mainly by the stomach, but also synthesized in the hypothalamus. This compound increases both GH release and food intake. The relative roles of hypothalamic and circulating ghrelin on GH secretion are still unknown. Endogenous ghrelin might amplify the basic pattern of GH secretion, optimizing somatotroph responsiveness to GH-releasing hormone. This peptide activates multiple interdependent intracellular pathways at the somatotroph, involving protein kinase C, protein kinase A and extracellular calcium systems. However, as ghrelin induces a greater release of GH in vivo, its main site of action is the hypothalamus. In this paper we review the available data on the discovery of ghrelin, the mechanisms of action and possible physiological roles of GH secretagogues and ghrelin on GH secretion, and, finally, the regulation of GH release in man after intravenous administration of these peptides.

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.

The influence of insulin on circulating ghrelin

2003 ◽  
Vol 284 (2) ◽  
pp. E313-E316 ◽  
Author(s):  
Daniel E. Flanagan ◽  
Mark L. Evans ◽  
Teresa P. Monsod ◽  
Frances Rife ◽  
Rubina A. Heptulla ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Energy Homeostasis ◽  
Insulin Infusion ◽  
Significant Rise ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Physiological Regulator ◽  
Underlying Mechanisms ◽  
Mean Glucose

Ghrelin is a novel peptide that acts on the growth hormone (GH) secretagogue receptor in the pituitary and hypothalamus. It may function as a third physiological regulator of GH secretion, along with GH-releasing hormone and somatostatin. In addition to the action of ghrelin on the GH axis, it appears to have a role in the determination of energy homeostasis. Although feeding suppresses ghrelin production and fasting stimulates ghrelin release, the underlying mechanisms controlling this process remain unclear. The purpose of this study was to test the hypotheses, by use of a stepped hyperinsulinemic eu- hypo- hyperglycemic glucose clamp, that either hyperinsulinemia or hypoglycemia may influence ghrelin production. Having been stable in the period before the clamp, ghrelin levels rapidly fell in response to insulin infusion during euglycemia (baseline ghrelin 207 ± 12 vs. 169 ± 10 fmol/ml at t = 30 min, P < 0.001). Ghrelin remained suppressed during subsequent periods of hypoglycemia (mean glucose 53 ± 2 mg/dl) and hyperglycemia (mean glucose 163 ± 6 mg/dl). Despite suppression of ghrelin, GH showed a significant rise during hypoglycemia (baseline 4.1 ± 1.3 vs. 28.2 ± 3.9 μg/l at t = 120 min, P < 0.001). Our data suggest that insulin may suppress circulating ghrelin independently of glucose, although glucose may have an additional effect. We conclude that the GH response seen during hypoglycemia is not regulated by circulating ghrelin.

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