Stimulated growth hormone (GH) secretion in children with delays in pubertal development before and after the onset of puberty: relationship with peripheral plasma GH-releasing hormone and somatostatin levels

1992 ◽  
Vol 74 (2) ◽  
pp. 272-278 ◽  
Author(s):  
G. Saggese
1995 ◽  
Vol 132 (6) ◽  
pp. 712-715 ◽  
Author(s):  
A Leal-Cerro ◽  
E Garcia ◽  
R Astorga ◽  
FF Casanueva ◽  
C Dieguez

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


2008 ◽  
Vol 33 (5) ◽  
pp. 880-887 ◽  
Author(s):  
Foued Ftaiti ◽  
Monem Jemni ◽  
Asma Kacem ◽  
Monia Ajina Zaouali ◽  
Zouhair Tabka ◽  
...  

The aim of this study was to differentiate the effects of hyperthermia and physical activity on circulating growth hormone (GH) secretion. Nine healthy volunteer adults performed two 40 min exercise trials and two 50 min passive standing trials. The exercise was performed in either thermo-neutral (N-Ex: air temperature 18 °C, air humidity 40%, and wet bulb globe temperature (WBGT) 17.7 °C) or hot environmental conditions (H-Ex: air temperature 33 °C, air humidity 30%, and WBGT 34.6 °C). The passive exposure trials were also performed in either a comfortable (N-P: air temperature 18 °C, air humidity 40%, and WBGT 17.7 °C) or a hot climatic chamber (H-P: air temperature 40 °C, air humidity 100%, and WBGT 97.1 °C). Plasma GH, plasma volume (PV), tympanic temperature (Tty), and body mass loss (BML) were measured before and after each trial. The decrease in PV was significantly higher during H-Ex and H-P sessions than during N-Ex and N-P sessions. Comparisons showed significantly lower BML in the N-Ex session (1.5% ± 0.3%) than in the H-Ex and H-P sessions (2.1% ± 0.3% and 1.9% ± 0.2%, respectively) (p < 0.001). The rise in Tty was significantly higher during the H-P session (2.9 ± 0.4 °C) (p < 0.001) when compared with the other sessions. Plasma GH concentration increased significantly during all the trials, particularly during the H-Ex session (45 ± 7 ng·mL–1) (p < 0.01). Both exercise and heat exposure, separately, are sufficient to increase significantly the plasma GH concentration, and their combined effect induced a highly synergistic rise in GH.


1994 ◽  
Vol 140 (3) ◽  
pp. 495-502 ◽  
Author(s):  
T P Fletcher ◽  
I J Clarke

Abstract This study examined the effect of thyroidectomy (TX) on the GH axis in sheep. The secretion of GH was monitored 10 and 77 days after TX or sham-TX when the effects on plasma GH and prolactin levels of the injection of 0·5 μg GH-releasing factor (GRF)/kg and 1 μg thyrotrophin-releasing hormone (TRH)/kg were also assessed. There were no significant differences in GH pulse amplitude, pulse frequency, inter-pulse interval and GH secreted/h between sham-TX and TX animals at 10 or 77 days after TX. There was no difference in the GH response to GRF injection in sham-TX sheep at any time but in TX sheep the GH response was significantly (P<0·05) attenuated 10 days after TX. After 77 days the GH response was similar to the response before TX. There was no measurable GH response to injection of TRH in sham-operated or TX sheep at any time. The prolactin response to TRH was not affected by TX or sham-TX. These results suggest that TX in sheep does not affect GH secretion but paradoxically the response to GRF is attenuated in hypothyroid sheep in the short term. TRH causes release of prolactin but not GH in sheep. Journal of Endocrinology (1994) 140, 495–502


1991 ◽  
Vol 125 (5) ◽  
pp. 487-490 ◽  
Author(s):  
Hajime Watanobe ◽  
Shinsuke Sasaki ◽  
Kazuo Takebe

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.


1993 ◽  
Vol 138 (2) ◽  
pp. 211-218 ◽  
Author(s):  
J. Muruais ◽  
A. Peñalva ◽  
C. Dieguez ◽  
F. F. Casanueva

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


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 ◽  
...  

2006 ◽  
Vol 50 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Ana Maria J. Lengyel

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.


1993 ◽  
Vol 128 (3) ◽  
pp. 197-201 ◽  
Author(s):  
Maria N Moreira-Andrés ◽  
Francisco J Cañizo ◽  
Federico Hawkins

The evaluation of growth hormone (GH) secretion is an important problem in pediatric endocrine practice. The diagnosis of GH insufficiency is based on the finding of a "blunted" GH response to GH provocative tests or on the demonstration of a decreased endogenous secretion. From a practical point of view, these methods are uncomfortable, expensive and time consuming. Recently, very sensitive specific assays to measure human GH in urine have been developed. We present a discussion of available data on these tests in order to estimate their role in the evaluation of a short or slowly growing child. The present available assays allow measuring very low levels of GH in a small sample of untreated urine. The main limitations of urinary GH measurement are the intrasubject variability, wide normal range, overlapping results in several GH secretory states and lack of information on GH pulsatility. However, most of these limitations also apply to other tests of GH secretion. The advantage of urinary GH tests is that they provide, in an easy procedure, information on serum GH concentration. There is good correlation between urinary and serum GH concentration and several findings suggest that urinary GH excretion reflects changes in plasma GH levels during the period of urine collection. Therefore, the usefulness of urinary GH measurement is that of a simpler and cheaper screening method for assessing integrated serum GH concentration in clinical practice.


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