Growth hormone release during insulin tolerance, Clonidine, arginine and growth hormone releasing hormone tests in short normal children and adolescents

1992 ◽  
Vol 15 (2) ◽  
pp. 131-135 ◽  
Author(s):  
L. Cavallo ◽  
A. Acquafredda ◽  
S. Liuzzi ◽  
R. Russo ◽  
C. Zecchino ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Children And Adolescents ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Releasing Hormone ◽  
Normal Children ◽  
Releasing Hormone ◽  
Insulin Tolerance

Effect of epoxyeicosatrienoic acids on growth hormone release from somatotrophs

1989 ◽  
Vol 256 (2) ◽  
pp. E221-E226 ◽  
Author(s):  
G. D. Snyder ◽  
P. Yadagiri ◽  
J. R. Falck
Keyword(s):  
Growth Hormone ◽  
Arachidonic Acid ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Epoxyeicosatrienoic Acids ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Releasing Hormone ◽  
Epoxyeicosatrienoic Acid ◽  
Releasing Hormone

Growth hormone secretion was stimulated in vitro by products of arachidonic acid epoxygenase, the epoxyeicosatrienoic acids. 5,6-Epoxyeicosatrienoic and 14,15-epoxyeicosatrienoic acid stimulated growth hormone release from an enriched population of somatotrophs (approximately 85%) by twofold. Inhibition of arachidonic acid metabolism by indomethacin did not affect growth hormone-releasing hormone stimulation of growth hormone release. In contrast, pretreatment of somatotrophs with an 11,12-isonitrile analogue of arachidonic acid that inhibits arachidonic acid epoxygenase, resulted in a 20-25% inhibition of growth hormone-releasing hormone-stimulated growth hormone release. 14,15-Epoxyeicosatrienoic acid stimulated a concentration-dependent increase (twofold) in the cytoplasmic concentration of adenosine 3',5'-cyclic monophosphate (cAMP) in the somatotrophs. 14,15-Epoxyeicosatrienoic acid also rapidly increased the intracellular free calcium concentration in somatotrophs from resting levels (approximately 80 nM) to greater than 250 nM. Growth hormone-releasing hormone increased the free intracellular calcium to 160-180 nM. Preincubation of somatotrophs with somatostatin inhibited growth hormone-releasing hormone-stimulated growth hormone secretion, cAMP accumulation, and 14,15-epoxyeicosatrienoic acid stimulated cAMP accumulation. These data are suggestive that the epoxyeicosatrienoic acids may have a role in the secretion of growth hormone.

Cholinergic Involvement in the Growth Hormone Releasing Hormone-Induced Growth Hormone Release: Studies in Normal and Acromegalic Subjects

1986 ◽  
Vol 43 (6) ◽  
pp. 670-675 ◽  
Author(s):  
Ferdinando Massara ◽  
Ezio Ghigo ◽  
Konstantinos Demislis ◽  
Domenico Tangolo ◽  
Enrico Mazza ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Release Studies

Somatostatin withdrawal alone is an ineffective generator of pulsatile growth hormone release in man

1993 ◽  
Vol 129 (5) ◽  
pp. 414-418 ◽  
Author(s):  
P Jean Ho ◽  
Gad B Kletter ◽  
Nancy J Hopwood ◽  
Roberta DeMott Friberg ◽  
Ariel L Barkan
Keyword(s):  
Growth Hormone ◽  
Gh Deficiency ◽  
Young Men ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Releasing Hormone ◽  
Gh Therapy ◽  
Releasing Hormone

To assess the relative roles of growth hormone-releasing hormone (GHRH) pulse and somatostatin withdrawal as potential generators of pulsatile growth hormone (GH) release in humans, we studied GH responses to iv bolus GHRH (1 μg/kg) and to termination of a 4 h iv somatostatin infusion (7.2 μg·kg−1·h−1) in five normal young men, and in five men with previously diagnosed isolated GH deficiency. The patients were diagnosed 8–15 years previously on the basis of typical auxological and hormonal criteria, were treated with exogenous GH and were off GH therapy for 1.5–8.9 years prior to this study. Growth hormone rises to a bolus GHRH were similar between the controls and the patients (maximum GH 27.3±15.3 vs 8.0±4.0 μg/l). The controls exhibited only a small GH rise to somatostatin withdrawal (maximum GH 2.9±1.2 μg/l), while the patients did not (maximum GH 0.7±0.1 μg/l; p<0.05). We conclude that somatostatin withdrawal by itself is an ineffective promoter of GH pulsatility. Periodic quiescence of somatostatinergic neurons must be associated with a concomitant GHRH pulse in order to result in a robust GH pulse.

Naloxone Inhibition of Postprandial Growth Hormone Releasing Hormone-Induced Growth Hormone Release in Obesity

1989 ◽  
Vol 50 (5) ◽  
pp. 529-532 ◽  
Author(s):  
Laura De Marinis ◽  
Antonio Mancini ◽  
Giuseppe Folli ◽  
Colomba D’Amico ◽  
Salvatore M. Corsello ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone
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