Repetitive Injections of GHRH in Normal Children and Adults

Sartório, Alessandro; Conti, Antonio; Spada, Anna; Faglia, G.

doi:10.1055/s-2007-1004959

Cited by 3 publications

(3 citation statements)

References 1 publication

(2 reference statements)

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“…In part at variance with the present findings are the results of studies performed in adult subjects in whom GHRH administration was found to inhibit the GH response to the second GHRH bolus (2). This phenome¬ non has been explained by an increase in the somatostatinergic tone secondary to GHRH administration, which antagonizes the action of the following GHRH challenge, but not that of the stimuli acting through inhibition of SRIH release such as arginine and pyridostigmine (5).…”

Section: Discussioncontrasting

confidence: 71%

“…In the last few years, several authors have demonstrated that the plasma GH response of adult subjects to acute GHRH stimulation is abolished by a previous GHRH injection ( 1,2). It has been speculated that an increase in the somatostatinergic tone following the first GHRH challenge might be responsible for the pituitary lack of response to the second stimulus.…”

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confidence: 99%

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GH response to GHRH, insulin, clonidine and arginine after GHRH pretreatment in children

Bernasconi

Volta²,

Cozzini³

et al. 1992

Acta Endocrinologica

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response to GHRH, insulin, clonidine and arginine after GHRH pretreatment in children. Acta Endocrinol 1992;126:105-8. ISSN 0001-5598 To determine whether differences in the neuroendocrine control of GH are present between children and adult subjects, the GH response to GHRH (1 \g=m\g/kg)(group 1), insulin-induced hypoglycemia (0.1 U/kg iv) (group 2), clonidine (150 \g=m\g/m2 po) (group 3) and iv arginine (0.5 g/kg in 30 min) (group 4) after GHRH pretreatment (1 \g=m\g/kg)was studied in 26 short-stature normal children (mean age 10.2 years). The results were compared with historical data in adults. No differences were present among mean peak GH levels after the first and second stimuli in groups 1, 2 and 3, while in group 4 the GH response to arginine administration was lower than that obtained after the initial GHRH (0.43 \m=+-\0.04 vs 0.9\m=+-\0.13nmol/l). Moreover, comparing the GH peak values following the second stimulus, it appears that the greatest GH responses were elicited by GHRH (1.31 \m=+-\0.23nmol/l) and clonidine (1.11\m=+-\0.22nmol/l), while the lowest was elicited by arginine (0.43\m=+-\0.04nmol/l). In adults, sequential GHRH administration leads to inhibition of the response of the somatotropes, probably mediated by an increase in hypothalamic somatostatin. Our results confirm that after GHRH prestimulation GHRH elicits a significant GH response suggesting that activation of the somatostatinergic tone is less effective in children. This hypothesis also explains the low GH response to arginine which acts selectively through somatostatin inhibition.In the last few years, several authors have demonstrated that the plasma GH response of adult subjects to acute GHRH stimulation is abolished by a previous GHRH injection ( 1, 2). It has been speculated that an increase in the somatostatinergic tone following the first GHRH challenge might be responsible for the pituitary lack of response to the second stimulus. This hypothesis has been further confirmed by studies in which it was shown that pyridostigmine, a cholinesterase inhibitor capable of reducing the somatostatin¬ ergic tone (3, 4), is effective in reinstating the GH responsiveness to repeated GHRH administration (5). The same mechanism has been advocated to explain the enhanced GH levels after GHRH pretreatment obtained by arginine, another somatostatin inhibiting agent (6), when injected either alone (7) or in combination with the second GHRH bolus (8).On the basis of this evidence, it has been suggested that stimuli eliciting a GH increase after GHRH pretreat¬ ment might act through mechanisms different from GHRH release and most likely involving somatostatin inhibition, as happens after insulin-induced hypogly¬ cemia (1) and, according to some authors (9), after clonidine.On the other hand, children show quite different GH responses to different stimuli. In fact, a persistent somatotrope responsiveness to repeated GHRH stimula¬ tion was demonstrated in this age group, suggesting that a discrete autoregulation of the somatostatin-mediated ...

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Section: Discussioncontrasting

confidence: 71%

mentioning

confidence: 99%

GH response to GHRH, insulin, clonidine and arginine after GHRH pretreatment in children

Bernasconi

Volta²,

Cozzini³

et al. 1992

Acta Endocrinologica

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“…The influence of adiposity on the neuroregulation of GH secretion in adults has been independently confirmed from the approximate entropy (ApEn) metric, which demonstrates greater irregularity of GH secretion in the obese, suggesting greater feedback activity within the axis [5][6][7]14]. In contrast, there are very few data on GH neuroregulation of overweight youth, and data from adults may not be directly applicable to youth because the neuroregulation of GH secretion likely differs in youth and adults [15,16].…”

Section: Introductionmentioning

confidence: 99%

Pubertal alterations in growth and body composition: IX. Altered spontaneous secretion and metabolic clearance of growth hormone in overweight youth

Roemmich¹,

Clark²,

Weltman³

et al. 2005

Metabolism

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Effects of oral glucose administration on spontaneous and growth hormone (GH)-releasing hormone-stimulated GH release in children and adults.

Valcavi¹,

Zini²,

Volta³

et al. 1994

The Journal of Clinical Endocrinology & Metabolism

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It has been suggested that hypothalamic regulation of GH secretion in children may differ from that in adults. On the other hand, there is evidence that oral glucose administration affects GH secretion through hypothalamic mechanisms. Therefore, we investigated spontaneous and GHRH-stimulated (1 microgram/kg BW) GH responses after oral glucose administration (children, 1.75 g/kg BW; adults, 75 g) in peripubertal normal children (13 girls and 13 boys, aged 11.7 +/- 0.4 yr; range, 8-13) and healthy adults (12 males and 14 females, aged 25.7 +/- 1.2 yr; range, 18-39). Three studies were carried out. In study 1, serum GH levels in 8 children were suppressed (< 1 microgram/L) for 135 min after oral glucose administration. Afterward, there was a rise in serum GH levels. In 8 adults, the suppressive effect of glucose persisted throughout the 210-min study period, and no GH rebound appeared. In study 2, the GH responses to iv GHRH boli in 10 adults and 10 children were, respectively, inhibited, unchanged, or augmented by an oral glucose load administered 30, 60, or 120 min before GHRH challenge. In study 3, oral glucose administration to 8 adults greatly enhanced the GH response to GHRH given 180 min after the glucose, whereas in 8 children, the GH response to GHRH was unchanged. In conclusion, glucose affects basal and GHRH-stimulated GH release in a similar manner in adults and children, indicating that neuroregulatory influences of glucose on the GH axis may not differ in the two age groups. In children, however, the duration of both the initial inhibitory and subsequent stimulatory effects of glucose administration on GH secretion is shorter.

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Repetitive Injections of GHRH in Normal Children and Adults

Cited by 3 publications

References 1 publication

GH response to GHRH, insulin, clonidine and arginine after GHRH pretreatment in children

GH response to GHRH, insulin, clonidine and arginine after GHRH pretreatment in children

Pubertal alterations in growth and body composition: IX. Altered spontaneous secretion and metabolic clearance of growth hormone in overweight youth

Effects of oral glucose administration on spontaneous and growth hormone (GH)-releasing hormone-stimulated GH release in children and adults.

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