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PubMed1998

Assessment of hypothalamic-pituitary function by hormonal pulsatility, gonadotropin-releasing hormone and thyrotropin-releasing hormone testing in women with euprolactinemic secondary amenorrhea.

To evaluate the integrated hypothalamic-pituitary function of euprolactinemic secondary amenorrhea, blood samples of 23 patients were taken every 15 min for 4 hours in examination of pulsatile LH, FSH, PRL secretions and then 2 hours GnRH, TRH tests were performed. Nine normal cycling women (group I) served as the controls. Thirteen amenorrheic women (group II) revealed responsive bleeding to progestin injection and the other 10 women (group III) were nonresponsive. The LH frequency, amplitude, and LH response to GnRH of groups II and I were comparable, whereas delta PRL after TRH in group II (60.8 +/- 18.9 ng/ml) exhibited a significantly (P < 0.05) exaggerated response, as compared with that of group I (43.6 +/- 11.4 ng/ml). The LH frequency (1.3 +/- 0.4/4h) and amplitude (1.7 +/- 0.4 mIU/mL) of group III were significantly lower (P < 0.01) than those in group I (2.4 +/- 0.5 and 2.5 +/- 0.5, respectively), but their delta LH and delta FSH responses to GnRH showed no differences from those of controls. The frequency, amplitude of PRL and delta PRL response to TRH in group III were no significant difference with those of group I. These results suggest that masked PRL hypersecretion and loss of the regulatory pulsatility of gonadotropin release may be responsible in part for the causes resulting to euprolactinemic secondary amenorrhea. The analysis of these hormonal environments is useful for the understanding of clinical perspectives, pathophysiology and management.

Adult↗
PubMed1999

Hexarelin-induced growth hormone response in short stature. Comparison with growth hormone-releasing hormone plus pyridostigmine and arginine plus estrogen.

UNLABELLED: Hexarelin (HEX) is a synthetic hexapeptide with strong GH-stimulating activity. We evaluated GH response (expressed as maximum value after stimulus [Cmax] and as area under the curve [AUC]) to HEX at the doses of 1 microg/kg i.v. (HEX 1) and 2 microg/kg i.v. (HEX 2), in comparison with the responses to GHRH (1 microg/kg i.v.) + pyridostigmine (PD, 60 mg po) and to arginine (ARG, 0.5 mg/kg i.v.) + ethinylestradiol (EE, 1 mg/day po for 3 days before the stimulation), in 5 subjects with familial short stature (FSS), 11 with constitutional growth delay (CGD), 6 with GH neurosecretory dysfunction (NSD), and 5 with isolated growth hormone deficiency (GHD). Cmax and AUC after HEX 1 were 26.8+/-10.5 ng/ml and 1448+/-514 ng/min x ml in FSS, 23.6+/-14.4 ng/ml and 1146+/-750 ng/min x ml in CGD, 36.9+/-21.5 ng/ml and 2048+/-1288 ng/min x ml in NSD, 9.4+/-5.8 ng/ml and 498+/-200 ng/min x ml in GHD (Cmax and AUC in FSS and CGD, p<0.05 vs GHD). Cmax and AUC after HEX 2 were 37.7+/-16 ng/ml and 1979+/-888 ng/min x ml in FSS, 32.5+/-16.2 ng/ml and 1613+/-237 ng/min x ml in CGD, 39.7+/-20.7 ng/ml and 2366+/-1569 ng/min xml in NSD, 13.4+/-4.2 ng/ml and 645+/-293 ng/min x ml in GHD (Cmax in FSS, CGD and NSD p<0.01 vs GHD; AUC in NSD, p<05 vs GHD). Cmax and AUC after GHRH+/-PD were 46.6+/-8.8 ng/ml and 3294+/-1031 ng/min x ml in FSS, 25.9+/-11.2 ng/ml and 1464+/-735 ng/min x ml in CGD, 38.8+/-21.7 ng/ml and 2428+/-1399 ng/min x ml in NSD, 8.4+/-6.2 ng/ml and 685+/-572 ng/min x ml in GHD (Cmax and AUC in FSS, p<0.001 vs CGD and GHD; Cmax in CGD and NSD, p<0.001 vs GHD). Cmax and AUC after ARG+EE were 21.3+/-4.2 ng/ml and 1432+/-514 ng/min x ml in FSS, 14.8+/-10 ng/ml and 805+/-489 ng/min x ml in CGD, 22.2+/-12.8 ng/ml and 1199+/-309 ng/min x ml in NSD, 4.6+/-2.5 ng/ml and 247+/-191 ng/min x ml in GHD (Cmax and AUC in FSS, CGD and NSD, p<0.01 vs GHD). Specificity was 62% for HEX 1 and 75% for HEX 2, GHRH+PD and ARG+EE. From a diagnostic point of view, HEX 1 + HEX 2 was the association with the largest percentage of false positives (20% in FSS, 27% in CGD and 33% in NSD), HEX 1 +GHRH+PD resulted in 9% in CGD, while the combined use of HEX 1 or HEX 2 with GHRH+PD or ARG+EE and of GHRH+PD with ARG+EE did not show false positive responses. IN CONCLUSION: I) the most effective dose of HEX was 2 microg/kg i.v.; 2) HEX did not show more specificity than GHRH+PD and ARG+EE; 3) the association of GHRH+PD with ARG+EE could yield the best results at lower costs, confirming these tests as first-line tools in evaluating GH secretion.

Adolescent↗
PubMed1991

Influence of naloxone infusion on prolactin and growth hormone response to growth hormone-releasing hormone in anorexia nervosa.

Anorexia nervosa (AN) is frequently associated with anomalies of growth hormone (GH) and prolactin (PRL) secretion. We studied the GH and PRL responses to GHRH1-44 (50 micrograms IV) and the effect of a naloxone infusion (1.6 mg/hr), started 1 hr before GHRH administration, on this response in 12 female patients with AN, aged 15-30 yr, and in seven normal women, aged 19-27 yr, during the follicular phase as controls. In AN, GHRH induced an increase in GH levels similar to that observed in normal subjects. A significant inhibition of the GH response to GHRH was observed during naloxone infusion, similar to the inhibition in normal female subjects during the follicular phase. PRL levels showed a significant increment after GHRH alone and a slight, nonsignificant, PRL increment after GHRH during naloxone infusion in AN patients. In contrast a slight PRL decrease was observed after GHRH, both before and during naloxone infusion, in the normal subjects. Our study demonstrates that endogenous opioids play a role in influencing PRL secretion in patients with AN different from their role in normal subjects.

Adolescent↗
PubMed2004

Temporal profile of beta follicle-stimulating hormone, beta luteinizing hormone, and growth hormone gene expression in the protandrous hermaphrodite, gilthead seabream, Sparus aurata.

The temporal profile of betaFSH, betaLH, and growth hormone (GH) gene expression was measured throughout the periods of gonadal development, spawning, and post-spawning in the protandrous hermaphrodite gilthead seabream (sb), Sparus aurata (L.). Sampling was carried out monthly, covering a 8-31 month fish age. Pituitary RNA was extracted individually. The levels of betaFSH, betaLH, and GH mRNA were measured by dot blot hybridization using sb betaFSH, betaLH, and GH cDNA as probes and analyzed by computing densitometer (values standardized using individuals' beta-actin pituitary mRNA levels). All three genes, betaFSH, betaLH, and GH were expressed throughout the year, with seasonal variations. However, transcript levels of betaLH were consistently higher than those of betaFSH. During the spawning season (which lasts for about 4 months), the mRNA levels of both betaFSH and betaLH subunits increased dramatically. betaFSH peaked at the start of the spawning season for both males and females, and was significantly higher in males. As for betaLH transcripts, a statistical interaction between sex and date was observed. No significant differences between males and females were found for GH. The pattern of GH expression levels was found to be correlated to that of betaLH.

Animals↗
PubMed2001

Serum luteinizing hormone, growth hormone and insulin-like growth factor-I after releasing hormone challenge in prepubertal ewe lambs selected for twinning.

Two studies evaluated hormonal markers as indicators of the onset of puberty in Debouillet sheep selected for twinning. In Trial 1, 29 ewe lambs (50 +/- 0.5 kg, 159 to 187 d of age) were given 10 microg GnRH (i.v.) on September 15 and blood was collected at 30 min intervals after the injection for 2 h. Additional samples were taken twice weekly and progesterone (P4) was measured. The day that serum P4 was greater than 1 ng/mL for 2 consecutive sampling days was classified as the day of puberty. Average day of puberty was October 12 (average age at puberty was 199 d) and ewes with values less or greater than the average were classified as early or late, respectively. Average weight at GnRH challenge was 50 kg and ewes weighing less or more were classified as light or heavy, respectively. Early ewes weighed more (P = 0.01) and reached puberty sooner (P = 0.01) than late ewes. Heavy lambs reached puberty earlier, weighed more at GnRH challenge, and had more LH area under the curve (AUC, P < 0.05) than light ewes. In Trial 2, we gave 27 ewe lambs (54 +/- 0.9 kg, 173 to 189 d of age) a single i.v. injection of 10 microg GnRH and 10 microg GHRH on September 17. Average day of puberty was October 13, average weight was 54 kg, and average age at puberty was 208 d. Categories were designated as described for Trial 1. Early lambs reached puberty sooner (P = 0.01) and weighed more (P = 0.01) than late lambs, but the puberty groups had similar LH AUC (P = 0.64) and GH AUC (P = 0.75), whereas IGF-I was greater (P = 0.01) in early puberty ewes than in late puberty ewes. Heavy lambs reached puberty earlier (P = 0.06), weighed more (P = 0.01), and tended (P = 0.11) to have more GH AUC than light ewes. No difference was observed in LH AUC or IGF-I between weight groups (P > 0.15). Results suggest that serum LH after GnRH is not a reliable indicator of the onset of puberty in ewe lambs selected for twinning, but heavier ewes tended to produce more GH after a GHRH challenge and reach puberty earlier than lighter ewe lambs.

Aging↗
PubMed1992

Synthesis of fully active biotinylated analogues of parathyroid hormone and parathyroid hormone-related protein as tools for the characterization of parathyroid hormone receptors.

The synthesis, purification, and characterization of biotinylated analogues of parathyroid hormone (PTH) and PTH-related protein (PTHrP) are described. A novel methodology was developed which allowed the selective biotinylation during solid-phase synthesis of either the Lys13 or Lys26 residue in PTH/PTHrP sequences. Incorporation of orthogonally protected N alpha-Boc-Lys(N epsilon-Fmoc) at a selected position in the sequence, followed by selective side-chain deprotection and biotinylation of the epsilon-amino group, permitted modification of the specific lysine only. Biotinylated analogues of [Nle8,18,Tyr34]bPTH(1-34)NH2 (analogue 1a) were prepared by modification of Lys13 with a biotinyl group (analogue 1) or a biotinyl-epsilon-aminohexanoyl group (analogue 2) or at Lys26 with a biotinyl-epsilon-aminohexanoyl group (analogue 3). A biotinylated PTHrP antagonist [Leu11,D-Trp12,Lys13(N epsilon-(biotinyl-beta-Ala))]PTHrP(7-34)NH2 (analogue 5), was also prepared. In a different synthetic approach, selective modification of the thiol group of [Cys35]PTHrP(1-35)NH2, in solution, with N-biotinyl-N'-(6-maleimidohexanoyl)hydrazide, resulted in analogue 4. The high affinities of the biotinylated analogues for PTH receptors present in human osteosarcoma B-10 cells or in porcine renal cortical membranes (PRCM), were comparable to those of the underivatized parent peptides. The analogues were also highly potent in stimulation of cAMP formation (analogues 1-4) or inhibition of PTH-stimulated adenylyl cyclase (analogue 5) in B-10 cells. The most potent analogue (analogue 1) had potencies in B-10 cells (Kb = 1.5 nM, Km = 0.35 nM) and in porcine renal membranes (Kb = 0.70 nM) identical or similar to those of its parent peptide, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Affinity Labels↗
PubMed1996

Growth hormone responses to growth hormone-releasing hormone and clonidine in patients with type I diabetes and in normal controls: effect of age, body mass index and sex.

OBJECTIVE: Increased plasma concentrations of GH and increased GH responses to provocative stimuli are reported in patients with poorly controlled type I diabetes and are suggested to be related to complications. Our aim was to investigate GH concentrations in moderately controlled patients. PATIENTS AND MEASUREMENTS: We have investigated IGF-I concentrations and fasting GH concentrations and the response to 1 microgram/kg body weight GH-releasing hormone (GHRH) intravenously and/or to 150 micrograms clonidine intravenously in 77 moderately controlled patients with type I diabetes and in 46 healthy controls. RESULTS: Median HbA1c in the patients was 8.5% (upper level of normal 6.3%). Fasting GH and GH concentrations after the administration of GHRH were not significantly different in patients with type I diabetes compared with normal controls. Fasting and stimulated GH concentrations after the administration of clonidine were significantly higher in the patients, but this could be explained by their lower age and body mass index compared with controls. In controls but not in patients there was a negative correlation between GH and glucose concentrations. IGF-I was significantly lower in patients with diabetes than in controls, even after correction for age, body mass index and sex. CONCLUSIONS: Patients with moderately controlled type I diabetes mellitus have normal baseline and stimulated GH concentrations after the administration of GHRH or clonidine compared with healthy controls, when corrected for age, body mass index and sex. However, these 'normal' GH concentrations must be considered inappropriately high in view of the hyperglycaemia in these patients. The low plasma IGF-I concentrations might be responsible for the GH over-production.

Adolescent↗
PubMed2000

Cholinergic modulation of growth hormone responses to growth hormone-releasing hormone in uraemic patients on peritoneal dialysis.

BACKGROUND: Hypothalamic cholinergic neurotransmission plays a major role in the regulation of GH secretion. Pyridostigmine, a cholinesterase inhibitor, is able to decrease hypothalamic somatostatinergic tone and release GH in normal subjects. Blockade of muscarinic receptor with pirenzepine blunts the GH release in several clinical situations. However, little information is available on the role played by central cholinergic pathways in GH regulation in uraemic patients. OBJECTIVE: We aimed to assess GH responses to GHRH after pretreatment with pyridostigmine and pirenzepine in a group of uraemic patients undergoing peritoneal dialysis (PD). GH responses of the patients treated with recombinant human erythropeitin (rhEPO) were compared to patients without treatment. DESIGN: We studied 14 male patients on PD and nine control subjects. All subjects underwent three endocrine test in random order after an overnight fast. Each subject received GHRH (100 microg, i.v. in bolus at 0 minutes). Sixty minutes before the injection of GHRH subjects were given oral placebo, pyridostigmine (120 mg), or pirenzepine (100 mg). MEASUREMENTS: Blood samples for GH were collected at -60, 0, 15, 30, 45, 60 and 90 minutes The hormonal secretory responses were studied by a time-averaged (area under the curves, AUC) and time-independent (peak values) analysis. RESULTS: Baseline GH concentrations were similar in patients and controls. GH responses to placebo plus GHRH were also comparable in patients and controls (peak 26.6 +/- 3.8 vs. 33.2 +/- 4.4 mU/l, AUC 28.2 +/- 3.4 vs. 27.8 +/- 4.6 mU/h/l). Pyridostigmine administration induced a significant potentiation of GH responses to GHRH both in patients (peak 43.2 +/- 5.2 mU/l, AUC 47.6 +/- 6.0 mU/h/l; P < 0.01) and in control subjects (peak 79.2 +/- 8.6 mU/l, AUC 78.0 +/- 9.4 mU/h/l; P < 0.01). However, the increment in GH peak and AUC was significantly (P < 0.05) greater in controls in relation to values found in patients. Pirenzepine administration induced an abolishment of GH release after GHRH stimulation both in PD patients (peak 5.4 +/- 2.6 mU/l, AUC 6.0 +/- 2.4 mU/h/l; P < 0.01) and in healthy controls (peak 3.8 +/- 0.6 mU/l, AUC 4.0 +/- 0.4 mU/h/l; P < 0.05). Responses to pyridostigmine plus GHRH and pirenzepine plus GHRH were similar in patients on chronic therapy with recombinant human erythropeitin and in patients without rhEPO therapy. CONCLUSION: These results suggest that the cholinergic regulation of GH release is preserved in uraemic patients on peritoneal dialysis. The significantly lower increase in GH response to GHRH induced by pyridostigmine suggests that cholinergic stimulatory tone is attenuated in patients in relation to control subjects. Long-term therapy with rhEPO seems not to affect GH responses to cholinergic stimulation or blockade.

Adult↗
PubMed1997

Targeted expression of constitutively active receptors for parathyroid hormone and parathyroid hormone-related peptide delays endochondral bone formation and rescues mice that lack parathyroid hormone-related peptide.

Mice in which the genes encoding the parathyroid hormone (PTH)-related peptide (PTHrP) or the PTH/PTHrP receptor have been ablated by homologous recombination show skeletal dysplasia due to accelerated endochondral bone formation, and die at birth or in utero, respectively. Skeletal abnormalities due to decelerated chondrocyte maturation are observed in transgenic mice where PTHrP expression is targeted to the growth plate, and in patients with Jansen metaphyseal chondrodysplasia, a rare genetic disorder caused by constitutively active PTH/PTHrP receptors. These and other findings thus indicate that PTHrP and its receptor are essential for chondrocyte differentiation. To further explore the role of the PTH/PTHrP receptor in this process, we generated transgenic mice in which expression of a constitutively active receptor, HKrk-H223R, was targeted to the growth plate by the rat alpha1 (II) collagen promoter. Two major goals were pursued: (i) to investigate how constitutively active PTH/PTHrP receptors affect the program of chondrocyte maturation; and (ii) to determine whether expression of the mutant receptor would correct the severe growth plate abnormalities of PTHrP-ablated mice (PTHrP-/-). The targeted expression of constitutively active PTH/PTHrP receptors led to delayed mineralization, decelerated conversion of proliferative chondrocytes into hypertrophic cells in skeletal segments that are formed by the endochondral process, and prolonged presence of hypertrophic chondrocytes with delay of vascular invasion. Furthermore, it corrected at birth the growth plate abnormalities of PTHrP-/- mice and allowed their prolonged survival. "Rescued" animals lacked tooth eruption and showed premature epiphyseal closure, indicating that both processes involve PTHrP. These findings suggest that rescued PTHrP-/- mice may gain considerable importance for studying the diverse, possibly tissue-specific role(s) of PTHrP in postnatal development.

Animals↗
PubMed1990

Pituitary luteinizing hormone (LH) and follicle-stimulating hormone (FSH) responses to gonadotropin-releasing hormone during the rat estrous cycle: an increased ratio of FSH to LH is secreted during the secondary FSH surge.

The hormonal interactions required for the generation of a secondary surge of FSH on the evening of proestrus have not been clearly defined. The role of GnRH in driving a surge of FSH has been questioned by findings in previous studies. In the current study, gonadotropin secretion was measured from pituitary fragments obtained from rats at 0900 and 2400 h on each day of the estrous cycle. Pituitary fragments were perifused in basal (unstimulated) conditions or in the presence of GnRH pulses to determine whether a selective increase in basal release of FSH and/or an increase in the responsiveness to GnRH occurs during the secondary FSH surge. Each anterior pituitary was cut into eighths and placed into a microchamber for perifusion. Seven pulses of GnRH (peak amplitude = 50 ng/ml; duration = approximately 2 min) were administered at a rate of one per hour starting at 30 min. Fractions of perfusate were collected every 5 min and frozen until RIA for LH and FSH. The mean total amount of LH or FSH secreted during the hour interval following each of the last six pulses of GnRH (or the corresponding basal hour) was calculated. Analysis of variance with repeated measures indicated that the evening secretion of LH on proestrus (2400 h) dropped significantly (p less than 0.05) from a maximum on the morning of proestrus (0900 h), whereas the FSH secretion remained elevated at this time. Therefore, the ratio of FSH to LH secreted in response to GnRH pulses was highest during the secondary FSH surge and lowest on the morning of proestrus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effects of steroid administration on pituitary luteinizing hormone and follicle-stimulating hormone in ovariectomized pony mares in the early spring: pituitary responsiveness to gonadotropin-releasing hormone and pituitary gonadotropin content.

These experiments tested the hypothesis that administration of steroid hormones to ovariectomized (OVX) mares during the vernal transition to the breeding season would influence LH and FSH secretion. Circulating gonadotropin concentrations, response to exogenous GnRH, and pituitary gonadotropin content were monitored. Experiments 1 and 2 were conducted, beginning 10 March, and 3 February, respectively, utilizing a total of 30 long-term OVX pony mares. In experiment 1, mares were administered vehicle (n = 5) or estradiol-17 beta (E2, n = 5, 5 mg/3 ml sesame oil), twice daily for 16 days. Blood samples were collected daily for assessment of circulating LH and FSH concentrations. On Day 10 of treatment, 400 micrograms GnRH were administered to all mares. LH increased significantly over days of treatment in the estradiol-treated group, but pituitary response to GnRH tended to be less than in control mares. Circulating FSH tended to decline over days of treatment in estradiol-treated mares, and the pituitary response to GnRH was significantly reduced. Pituitary LH, but not FSH, was increased on Day 16 of treatment with estradiol. In experiment 2, 20 OVX mares received, twice daily, vehicle (n = 5), E2, n = 5; 5 mg), progesterone (P4, n = 5; 100 mg), or progesterone plus estradiol (P4/E2, n = 5; 100 + 5 mg). Treatment continued for 14 days. GnRH (100 micrograms) challenges were administered on Days 6 and 13 of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Anestrus↗
PubMed1986

The effect of oxandrolone on the growth hormone response to growth hormone releasing hormone in children with constitutional growth delay.

The effect of treatment with oxandrolone, an anabolic steroid, on GH response to GH-releasing hormone (GHRH) has been evaluated in children with constitutional growth delay. Five subjects, four males and one female, aged 11.0-17.1 years were given oxandrolone 0.1 mg/kg p.o. daily for 2 months, and underwent acute administration of GHRH (GRF 1-40, 1 microgram/kg i.v.) before and after withdrawal of oxandrolone therapy. GHRH administration induced a much greater GH response, evaluated either as a peak plasma GH levels or plasma GH integrated area, after than it did before oxandrolone treatment. These findings indicate that in children with constitutional growth delay oxandrolone increases the sensitivity of somatotrophs to exogenous GHRH and, likely, to the endogenously-released neurohormone.

Adolescent↗
PubMed1986

Nocturnal pulsatile growth hormone releasing hormone treatment in growth hormone deficiency.

We have treated five GH-deficient prepubertal children (4 M, 1 F) with GH releasing hormone 1-40 (GHRH1-40) in two dosage regimens over 9 months. Profiles of serum GH concentrations were obtained over 24 hours before treatment and nocturnal profiles were obtained serially throughout the study. GHRH was administered subcutaneously at night for four pulses using 1 microgram/kg/pulse in the first 3 months and 2 micrograms/kg/pulse for a further 6 months. All subjects demonstrated pituitary responsiveness to i.v. GHRH before treatment and at 3 and 6 months. GH secretion was induced in a pulsatile fashion in response to subcutaneous GHRH in three children from the first night of treatment. A self priming effect to successive GHRH pulses was evident and the response augmented with time and with the higher dose regimen. The growth velocity of these three children increased from a mean of 3.7 cm/year (range 3.7-3.8) before treatment to 5.5 cm/year (range 4.1-7.2) over the first 3 months and to 7.2 cm/year (range 4.8-9.2) over the following 6 months. In one subject entrainment of GH secretion to GHRH did not occur until the higher dose regimen and this was associated with a modest increase in growth velocity. One subject did not respond to treatment. Pulsatile administration of GHRH1-40 is effective in inducing GH secretion and promoting growth acceleration in some children with idiopathic GH deficiency. The optimal dose and mode of administration of GHRH have yet to be established.

Child↗
PubMed1987

Reduced growth hormone response to growth hormone-releasing hormone in children with simple obesity: evidence for somatomedin-C mediated inhibition.

We have evaluated the plasma GH response to a single injection of 1 microgram/kg of GH-releasing hormone (GHRH)-40 in 15 obese children and 15 age-matched control children. Most of the obese children showed a subnormal plasma GH response to GHRH and the mean plasma GH integrated area (IC-GH) following stimulation was significantly smaller in obese than control children. Plasma somatomedin-C (SM-C) levels were significantly higher in obese than control children, and were negatively correlated with the peak plasma GH levels (r = -0.616, P less than 0.01) and the IC-GH (r = -0.554, P less than 0.02) after GHRH. Non-esterified fatty acids (NEFA) and fasting plasma insulin levels were also elevated in obese children, but did not correlate with the extent of plasma GH response to GHRH. These data confirm previous observations on the refractoriness of obese children to release GH after GHRH, and imply that it may be due to the feedback inhibition operated by the elevated plasma levels of SM-C.

Body Weight↗
PubMed1987

Stilboestrol pretreatment of children with short stature does not affect the growth hormone response to growth hormone-releasing hormone.

Oestrogens are known to enhance both basal and stimulated GH secretion. To examine whether this effect is mediated through the hypothalamus or the pituitary we performed insulin tolerance and GH-releasing hormone (GHRH) tests with and without oestrogen priming in a group of 14 short children. Pretreatment with stilboestrol increased basal levels of GH and both peak and incremental levels during insulin hypoglycaemia. In contrast, there was no effect of stilboestrol priming on the GH response to either an i.v. bolus of 100 micrograms or 0.1 microgram/kg (range 2-6 microgram) of GHRH. The children had significantly higher GH responses to an unprimed GHRH than unprimed insulin tolerance test. We conclude stilboestrol priming acts through the hypothalamus presumably by increasing endogenous GHRH release, and that short children with a subnormal GH response to insulin hypoglycaemia show a greater response to GHRH; this suggests the presence of a hypothalamic cause for their decreased GH secretion.

Body Height↗
PubMed1993

Melatonin stimulates growth hormone secretion through pathways other than the growth hormone-releasing hormone.

OBJECTIVE: There is evidence that melatonin plays a role in the regulation of GH secretion. The aim of this study was to investigate the neuroendocrine mechanisms by which melatonin modulates GH secretion. Thus we assessed the effect of oral melatonin on the GH responses to GHRH administration and compared the effects of melatonin with those of pyridostigmine, a cholinergic agonist drug which is likely to suppress hypothalamic somatostatin release. DESIGN: The study consisted of four protocols carried out during the afternoon hours. Study 1: oral melatonin (10 mg) or placebo were administered 60 minutes prior to GHRH (100 micrograms i.v. bolus). Study 2: GHRH (100 micrograms i.v. bolus) or placebo were administered at 0 minutes; oral melatonin or placebo were given at 60 minutes and were followed by a second GHRH stimulus (100 micrograms i.v. bolus) at 120 minutes. Study 3: placebo; oral melatonin (10 mg); oral pyridostigmine (120 mg); melatonin (10 mg) plus pyridostigmine (120 mg) were administered on separate occasions. Study 4: placebo; oral melatonin (10 mg); oral pyridostigmine (120 mg); melatonin (10 mg) plus pyridostigmine (120 mg) were administered on separate occasions 60 minutes prior to a submaximal dose (3 micrograms i.v. bolus) of GHRH. SUBJECTS: Four groups of eight normal male subjects, ages 22-35 years, were randomly assigned to each protocol. MEASUREMENTS: Growth hormone was measured by RIA at 15-minute intervals. RESULTS: Oral melatonin administration had a weak stimulatory effect on GH basal levels. Prior melatonin administration approximately doubled the GH release induced by supramaximal (100 micrograms) or submaximal (3 micrograms) doses of GHRH. Melatonin administration restored the GH response to a second GHRH challenge, given 120 minutes after a first GHRH i.v. bolus. The GH releasing effects of pyridostigmine, either alone or followed by GHRH, were greater than those of melatonin. However, the simultaneous administration of melatonin and pyridostigmine was not followed by any further enhancement of GH release, either in the absence or in the presence of exogenous GHRH. CONCLUSIONS: Our data indicate that oral administration of melatonin to normal human males increases basal GH release and GH responsiveness to GHRH through the same pathways as pyridostigmine. Therefore it is likely that melatonin plays this facilitatory role at the hypothalamic level by inhibiting endogenous somatostatin release, although with a lower potency than pyridostigmine. The physiological role of melatonin in GH neuroregulation remains to be established.

Administration, Oral↗
PubMed1989

Use of continuous subcutaneous growth hormone-releasing hormone (GHRH (1-29)NH2) infusions to augment growth hormone secretion and to promote growth.

It has previously been shown that an 8-day continuous subcutaneous infusion of GHRH (1-29)NH2 in adult males augments growth hormone (GH) secretion with no evidence of desensitization of the response. The present report details the results of treatment with continuous subcutaneous infusions of GHRH (1-29)NH2 in eight children aged 6-9 years with partial GH insufficiency. All the children showed augmentation of GH secretion and an increase in growth velocity after 3 and 6 months of therapy.

Child↗
PubMed1991

Exogenous growth hormone inhibits bovine but not murine pituitary growth hormone secretion in vitro: evidence for a direct feedback of growth hormone on the pituitary.

To test the hypothesis that one aspect of growth hormone (GH) regulation involves a direct effect of GH on its own secretion at the level of the pituitary, we evaluated the effects of human GH on basal and GH-releasing factor (GRF)-induced GH secretion in rat and bovine pituitary cell cultures. Both 4 h (acute) and 24 h (chronic) exposure of bovine pituitary cells to exogenous human GH significantly (p less than 0.001) reduced GH secretion. Acute treatment resulted in a decrease in GH secretion from 579 +/- 24 to 500 +/- 17 ng/ml 4 h (mean +/- SEM, n = 24) while chronic treatment resulted in a GH decrease from 595 +/- 21 to 483 +/- 17 ng/ml/4 h. In contrast, human GH treatment of rat somatotropes had no effect on basal GH secretion. GRF-stimulated GH secretion was not affected by either acute or chronic GH exposure in either species. These results demonstrate that there are species-specific differences in the ability of GH to regulate its own secretion and provide evidence for a direct inhibitory effect of GH at the level of the bovine pituitary.

Animals↗