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PubMed1986

Exogenous growth hormone inhibits growth hormone-releasing factor-induced growth hormone secretion in normal men.

Previous studies from this laboratory and by others in rats, monkeys, and humans support the concept that growth hormone (GH) can regulate its own secretion through an autofeedback mechanism. With the availability of human growth hormone-releasing factor (GRF), the possible existence of such a mechanism was reexplored by examining the effect of exogenous GH on the GH response induced by GRF-44-NH2 in six normal men (mean age, 32.4 yr). In all subjects the plasma GH response evoked by GRF-44-NH2 (1 microgram/kg i.v. bolus) was studied before and after 5 d of placebo (1 ml normal saline i.m. every 12 h), and then before and 12 h after 5 d of biosynthetic methionyl human GH (5 U i.m. every 12 h). The GH response to GRF (maximal increment over time 0 value) was significantly inhibited after GH treatment (0-1.3 vs. 2.3-11.2 ng/ml before treatment, P = 0.05), but was not significantly affected by placebo. This impaired pituitary response to GRF persisted for at least 24 h following exogenous GH treatment in two subjects who underwent further study. Serum somatomedin-C concentrations were significantly increased after 5 d of GH treatment (2.66-5.00 vs. 0.92-1.91 U/ml before treatment, P = less than 0.01). The impaired pituitary response to GRF may be mediated indirectly through somatomedin, somatostatin, by a direct effect of GH on the pituitary somatotropes, or by all of these mechanisms. These data suggest that after GH treatment, the blunted GH response to synthetic GRF is not solely a consequence of the inhibition of hypothalamic GRF secretion.

Adult↗
PubMed1994

Growth hormone response to growth hormone-releasing hormone stimulation in oligozoospermic patients.

OBJECTIVE: To evaluate the GH response to growth hormone-releasing hormone (GH-RH) stimulation in oligozoospermic men. SETTING: Outpatient Clinic of Andrology at the Fundación Puigvert and the Department of Clinical Chemistry, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain. PATIENTS: Fifteen oligozoospermic patients and 15 normozoospermic fertile men matched for age and body mass index. INTERVENTION: Endocrine status was determined by assay of basal levels of gonadotropins (FSH, LH), T, E2, inhibin, and insulin-like growth factor I (IGF-I). Serum GH levels were measured before and after GH-RH administration. RESULTS: GH response to GH-RH was significantly greater in patients than in controls. There was a positive correlation between the GH response and IGF-I levels in oligozoospermic patients only. Regression analysis showed a significant negative association of GH peak with inhibin after controlling for IGF-I in oligozoospermic patients. CONCLUSION: The results indicate that there is an altered responsiveness of pituitary to GH-RH administration in oligozoospermic patients; this did not appear to be due to the influence of gonadal steroid levels but rather to inhibin or some related peptide.

Adult↗
PubMed1991

Altered growth hormone response after growth hormone releasing hormone administration in chronic renal failure.

Eleven chronic renal failure patients and 11 matched controls, received growth hormone GHRH (1 microgram/kg iv) or TRH (400 microgram iv) on separate occasions, immediately before undergoing hemodialysis. GHRH-induced GH peak in uremics (22.7 +/- 5.2 micrograms/l) was not different from that obtained in control subjects (16.0 +/- 4.3 micrograms/l). However, the uremic patients did not show the habitual post-peak fall, remaining GH levels over 10 micrograms/l till the end of the test. Differences between the two groups were significant (p less than 0.05). Uremic patients showed PRL values higher than in controls, however their TRH-induced PRL peak (20.6 +/- 6.6 micrograms/l) was not different from that of controls (26.5 +/- 3.0 micrograms/l). Again chronic renal failure patients showed PRL plasma values abnormally elevated till the end of the test. Differences between the two groups were significant (p less than 0.05). Administration of placebo to a different group of seven uremic patients did not alter GH and PRL plasma levels. This sustained secretion of both GH and PRL in uremia could be attributed to reduced kidney clearance. However, when subjects were examined individually both the GHRH- and the TRH-induced hormonal peaks and the subsequent fall were not different in both groups. Unlike with controls, in uremic patients GHRH-stimulated GH and TRH-stimulated PRL/GH peaks were dispersed throughout the 120 min period. In controls GH and PRL peaks clustered around 15-30 min. The peak dispersion created a false impression of flattened curves or sustained hypersecretion in uremia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Stimulation of growth hormone secretion in dwarf chickens by thyrotrophin-releasing hormone (TRH) or human pancreatic growth-hormone-releasing factor (hpGRF).

The basal plasma growth hormone (GH) level in adult sex-linked dwarf hens was elevated in comparison with autosomal dwarf hens and with control (Cornell K strain) laying hens. The iv administration of thyrotrophin-releasing hormone (TRH) (10 micrograms/kg) had no effect on GH secretion in control hens but slightly (1.2-fold) and transiently (for 10 min) increased the GH level in the autosomal dwarfs and greatly (8.7-fold) increased the GH level in the sex-linked dwarfs, in which it remained elevated for at least 30 min after injection. The iv administration of human pancreatic GH-releasing factor (hpGRF) (10 micrograms/kg) stimulated GH release in each strain. The response in the sex-linked dwarfs was greater than that in the autosomal dwarfs and the control hens but less than that elicited by TRH. These results suggest that the increased basal GH level in the sex-linked dwarfs results from an increased responsiveness to provocative stimulation.

Animals↗
PubMed1989

Somatostatin inhibition of thyrotropin-releasing hormone- and growth hormone-releasing factor-induced growth hormone secretion in young and adult anesthetized chickens.

The present communication examines the influence of somatostatin (SRIF14) on basal and thyrotropin-releasing hormone (TRH)- or growth hormone-releasing factor (GRF)-induced GH secretion in young (6 week old) and adult male chickens. Studies were performed in sodium pentobarbitone-anesthetized chickens where basal plasma concentrations of GH are low and both TRH and GRF consistently stimulate GH release. In both young and adult chickens, basal GH secretion was reduced by SRIF14 infusion (3 micrograms/kg/min). Similarly, in adult and young birds, the GH secretory response to a challenge with a GRF bolus (10 micrograms/kg) was inhibited by the concomitant intravenous infusion of SRIF14 (0.3 or 3.0 micrograms/kg/min). In adult chickens, the GH response to TRH (10 micrograms/kg) was suppressed (by 93%) by SRIF14 infusion (3 micrograms/kg/min) and tended to be inhibited (by 29%) by a lower dose of SRIF14 (0.3 micrograms/kg/min). In contrast, in young chicks, GH release following TRH challenge (either 1 or 10 micrograms/kg) was only partially inhibited by SRIF14 infusion (3 micrograms/kg/min). The response to a TRH challenge (10 micrograms/kg) was unaffected by the low dosage of SRIF14 infusion (0.3 micrograms/kg/min). It is concluded that SRIF14 inhibits both GRF- and TRH-stimulated GH release in young and adult chickens.

Aging↗
PubMed1990

The growth hormone clamp technique: inhibition of growth hormone release by growth hormone occurs independently of free fatty acids.

It has been suggested that growth hormone (GH) can inhibit its own release: in fact it has repeatedly been shown that an acute methionyl-GH (met-GH) infusion blocks the GH response to GH-releasing hormone (GHRH). However, met-GH infusions are accompanied by a significant increase of free fatty acids (FFA), which can block GH release. The aim of this study was to evaluate whether the inhibition of GH response to GHRH also occurs when lipolysis is pharmacologically blocked. Therefore, six normal subjects received GHRH, 50 micrograms intravenously (IV), after a 4-hour saline infusion and a 4-hour met-GH infusion (80 ng/kg/min, yielding a constant GH level of 33.6 +/- 4.63 micrograms/L), and GH release was evaluated during the following 2 hours. To prevent lipolysis, all subjects received on both occasions acipimox, an antilipolytic agent, 500 mg during the 6 hours before IV GHRH. GHRH induced a clear GH release during saline infusion (46.6 +/- 2.70 micrograms/L) and a scanty GH release during met-GH infusion (9.3 +/- 1.52 micrograms/L; P less than .01). Plasma levels of FFA, somatostatin, insulin-like growth factor I (IGF-I), and glucagon and serum insulin levels were unaffected, while blood glucose levels slightly decreased during saline infusion, but not during GH infusion. These data confirm that met-GH inhibits GHRH-induced GH release, and demonstrate that this inhibition is not mediated by FFA levels.

Adult↗
PubMed1992

Effect of galanin on the growth hormone response to growth hormone-releasing hormone in acromegaly.

Galanin enhances growth hormone (GH)-releasing hormone (GHRH)-stimulated GH secretion in normal man. In acromegaly, circulating GH levels are increased and the GH response to GHRH may be exaggerated. Galanin has been recently shown to decrease circulating GH levels in acromegaly. The aim of our study was to investigate the effects of galanin on the GH response to GHRH in acromegalic subjects. Five acromegalic patients (three men and two women) and seven healthy adult subjects (five men and two women) were studied. GHRH-induced GH secretion was evaluated during a 40-minute intravenous (IV) infusion of saline (100 mL) or porcine galanin (12.5 micrograms/min in 100 mL saline). In normal subjects, delta GH levels after GHRH+porcine galanin administration (47 +/- 7.5 micrograms/L) were significantly higher in comparison to levels obtained with GHRH+saline (21.7 +/- 3.5 micrograms/L, P < .05). In acromegalic patients, GH responses to GHRH (delta GH, 18.8 +/- 8.6 micrograms/L) were not altered by galanin infusion (delta GH, 17.6 +/- 5 micrograms/L). Our results give the first evidence that the same dose of galanin that induces a significant enhancement of the GH response to GHRH in normal subjects has no effect on the GH response to GHRH in acromegalic patients. It can be hypothesized that galanin may interact at the pituitary level with its own receptors expressed by somatotropes independent of GHRH. Failure of galanin to enhance GH response to GHRH in acromegalic patients could be due to a change in function of the galanin receptor on GH-secreting adenomatous cells.

Acromegaly↗
PubMed1994

Thyrotropin-releasing hormone: inhibitory function on growth hormone through both somatostatin and growth hormone-releasing factor neurons.

Double labelling immunohistochemistry using antibodies to thyrotropin releasing hormone (TRH) and somatostatin (SS) was undertaken in the anterior hypothalamus in 6 rats. Light microscopic quantitation revealed that 94.5% of SS immunopositive perikarya in the preoptic anterior hypothalamic area (PO/AHA) and 97.5% in the paraventricular nucleus appeared to be contacted by one or more TRH immunopositive terminals. In the chronically cannulated unanaesthetised male rat, unilateral microinjections of a range of doses of TRH were made in the PO/AHA, where SS neurons are located, or in the medial basal hypothalamus, where growth hormone (GH)-releasing factor (GRF) neurons are located. Transient reductions in GH plasma levels occurred only after injections of the highest (10 nmol) dose of TRH in both sites. The function of TRH inputs to both somatostatin and GRF neurons appears to be inhibitory for GH. The physiological conditions in which these inputs function remain to be defined.

Animals↗
PubMed1994

Lack of involvement of the cholinergic mechanism in vasoactive intestinal peptide- and peptide-histidine methionine-induced growth hormone (GH) responses in acromegaly: comparison with the GH responses to thyrotropin-releasing hormone and GH-releasing hormone.

We examined whether the cholinergic mechanism is involved in the paradoxical GH responses to vasoactive intestinal peptide (VIP) and peptide histidine methionine (PHM) in acromegaly. 28 patients with active acromegaly underwent i.v. bolus injections of thyrotropin-releasing hormone (TRH, 500 micrograms), GH-releasing hormone (GHRH, 100 micrograms), VIP (100 micrograms), and PHM (100 micrograms) with or without a prior atropine treatment (1 mg, i.m., 30 min before). Blood samples were collected before and at intervals up to 120 min after the injection, and plasma GH levels were measured. In response to TRH, GHRH, VIP and PHM, 23 (82%), 24 (86%), 13 (46%) and 7 (25%) patients, respectively, responded with a significant GH increase (> 50% and 6 micrograms/l above the basal level). The effect of atropine pretreatment was examined in only these responders to the respective peptides. When the GH responses were estimated by the area under the response curve, the atropine pretreatment was able to significantly suppress the GH response to GHRH, but not to TRH, VIP, or PHM. Although the lack of cholinergic involvement in the TRH-induced GH release in acromegaly is confirmatory to previous reports, the same results with the VIP- and PHM-induced GH release are novel. The present study may suggest that in acromegaly the physiological GH response is mediated by the cholinergic mechanism, but the paradoxical ones are not.

Acetylcholine↗
PubMed2000

Structure and activities of constrained analogues of human parathyroid hormone and parathyroid hormone-related peptide: implications for receptor-activating conformations of the hormones.

Parathyroid hormone (PTH) has a helix-bend-helix structure in solution. Part of the C-terminal helix, residues 21-31, is amphiphilic and forms a critical receptor-binding region. Stabilization of this alpha-helix by lactam formation between residues spaced i, i + 4 on the polar face was previously reported to increase adenylyl cyclase-stimulating (AC) activity if between residues 22 and 26 but to diminish it if between residues 26 and 30 [Barbier et al. (1997) J. Med. Chem. 40, 1373-1380]. This work reports the effects of other cyclizations on the polar face, differing in ring size or position, on alpha-helix conformation, as measured by circular dichroism, and on AC-stimulating activity. All analogues cyclized between residues 22 and 26 had at least a 1. 5-fold increase in activity, suggesting an alpha-helical structure between about residues 21 and 26. Cyclization between residues 25 and 29 or residues 26 and 30 diminished activity by 20-30%, despite stabilizing alpha-helix, suggesting that residues 25-31 bind to the receptor in a helical, but not classical alpha-helical, conformation. Analogues cyclized between residues 13 and 17 had slightly increased activity. A bicyclic analogue, with lactams between residues 13 and 17 and residues 22 and 26, had about the same activity as that cyclized only between 22 and 26. Parathyroid hormone-related peptide (PTHrP) may bind in a manner similar to the common receptor, but hydrophobic moment calculations suggest that it must bind as a tighter helix in order to optimally present its hydrophobic residues to the receptor. Both PTHrP analogues cyclized between either residues 22 and 26 or residues 26 and 30 had more stable alpha-helices but reduced AC activities, consistent with this hypothesis.

Adenylyl Cyclases↗
PubMed1996

Developmental potential of embryos produced by in-vitro fertilization from gonadotrophin-releasing hormone antagonist-treated macaques stimulated with recombinant human follicle stimulating hormone alone or in combination with luteinizing hormone.

We previously demonstrated, in luteinizing hormone (LH)-deficient macaques, that follicular growth and maturation occurred with administration of exogenous (recombinant human) follicle stimulating hormone (r-hFSH) alone, and that the oocytes recovered fertilized at a notably higher rate than their counterparts from animals receiving both r-hFSH and r-hLH (Zelinski-Wooten et al., 1995). Here, the developmental potential of embryos produced from animals treated with r-hFSH alone or in combination with r-hLH was evaluated. Embryos (n = 127) were cryopreserved, thawed and either co-cultured on buffalo rat liver cells until the hatched blastocyst stage or transferred to synchronized recipients. Although embryos from each treatment group demonstrated a similar ability to develop to hatched blastocysts with a definitive inner cell mass, a significant difference was seen in cryosurvival (56 versus 78%) and in developmental rate to the hatched blastocyst (12 versus 10 days) between embryos from the r-hFSH alone and the combination group respectively. Pregnancies resulted following oviductal embryo transfers in both groups, with corpus luteum rescue occurring on days 12-16 of the luteal phase. In summary, r-hFSH alone during the pre-ovulatory interval is adequate for the gametogenic events required to produce embryos that develop either in vitro or in vivo; however, exposure to r-hLH may improve embryo viability and the rate of development.

Animals↗
PubMed2004

Dose-finding study of daily gonadotropin-releasing hormone (GnRH) antagonist for the prevention of premature luteinizing hormone surges in IVF/ICSI patients: antide and hormone levels.

BACKGROUND: The aim of this study was to define the minimal effective dose of antide (Iturelix) to prevent premature luteinizing hormone (LH) surges in in vitro fertilization (IVF) patients. METHODS: In a prospective, single centre study, 144 IVF/ICSI patients were stimulated with r-hFSH from cycle day 2 and from cycle day 6 onwards, cotreated with daily 2 mg/2 ml (n=30), 1 mg/ml (n=30), 0.5 mg/ml (n=31), 0.5 mg/0.5 ml (n=23) and 0.25 mg/ml (n=30) GnRH antagonist (antide). Serum samples were taken three times daily during antide administration to assess antide and hormone levels. The minimal effective dose was defined as the lowest dose group with <2 LH surges (LH >12.4 IU/l and progesterone >2 ng/ml). RESULTS: Serum antide levels, mean LH and E2 levels per day and their area under the curves were dose-related to antide. The bioavailability of antide almost doubled after dilution in larger volumes. Pre-injection LH levels gradually increased during GnRH antagonist treatment. LH surges occurred in the lowest dose groups 0.5 mg/ml (3.2%), 0.5 mg/0.5 ml (6.7%) and 0.25 mg/ml (13.3%). Hence, 0.5 mg/ml is considered to be the minimal effective dose. Antide was overall well tolerated and safe. CONCLUSIONS: 0.5 mg/ml antide is the minimal effective dose to prevent an untimely LH surge in IVF patients stimulated with r-hFSH.

Adult↗
PubMed2002

Estradiol modulation of growth hormone secretion in the ewe: no growth hormone-releasing hormone neurons and few somatotropes express estradiol receptor alpha.

Evidence suggests that estrogen modulates growth hormone (GH) release and that GH plays an important role in follicular and ovulatory processes. How estradiol affects GH secretion is unclear. Having verified that there is a coincident surge of GH at the time of the preovulatory LH surge, immunocytochemical studies incorporating high-temperature antigen retrieval were used to determine whether GH-releasing hormone (GHRH) neurons, somatotropes, or both, expressed estrogen receptor alpha (ER), in the ewe. Although GHRH neurons were surrounded by many ER cells, they did not express immunocytochemically detectable ERs. In contrast to gonadotropes, in which the majority expressed ERs, few somatotropes were estrogen receptive. These data suggest that estrogen does not act directly on GHRH neurons to influence GH secretion, and any direct effect on pituitary GH release, through the ERalpha, may be small.

Animals↗
PubMed1986

Human pancreatic growth hormone releasing hormone fails to stimulate human growth hormone both in Cushing's disease and in Cushing's syndrome due to adrenocortical adenoma.

An absent or severely blunted hGH response to an i.v. bolus injection (100 micrograms) of human pancreatic growth hormone releasing hormone (hpGRF 1-44) was found in seven female patients with Cushing's syndrome (five with pituitary dependent Cushing's disease and two due to an adrenal adenoma) and four men with pituitary dependent Cushing's disease. Three of the female and three of the male patients had an adequate hypoglycaemia after insulin administration. All these patients showed an absent or blunted hGH response after insulin induced hypoglycaemia. The GHRH data in these patients are in agreement with those in older literature on hGH responsiveness to stimuli such as L-dopa, arginine and insulin induced hypoglycaemia. It is concluded that hypercortisolism inhibits hGH release to various stimuli at the pituitary level.

Adenoma↗
PubMed1984

Comparative stimulation of growth hormone secretion in anaesthetized chickens by human pancreatic growth hormone-releasing factor (hpGRF) and thyrotrophin-releasing hormone (TRH).

Plasma concentrations of growth hormone (GH) were elevated in anaesthetized male domestic fowl following the intravenous administration of either synthetic human pancreatic GH-releasing factor 1-44 (NH2) (hpGRF) or synthetic thyrotrophin-releasing hormone (TRH). In 6-week-old chicks the plasma GH level was elevated between 5 and 10 min after the injection of hpGRF at doses between 1 and 80 micrograms/kg. The magnitude of the response increased with doses of hpGRF between 1 and 10 micrograms/kg but declined with higher doses. The GH concentration rapidly declined between 10 and 20 min and between 20 and 40 min after injection. The administration of TRH had similar effects on GH secretion, although the responses were greater than with comparable doses of hpGRF, and the most effective dose (1-1.4 micrograms/kg) was less than with hpGRF. In anaesthetized adult cockerels GH secretion was also increased by the administration of hpGRF (1-20 micrograms/kg) or TRH (0.1-80 micrograms/kg) and in both cases the dose-response relationship was biphasic. The maximal response to TRH in adult birds was again greater than that produced by hpGRF although the response was less than that elicited in immature birds and required a higher dose (20 micrograms/kg) of TRH. The optimal dose of hpGRF and the magnitude of the GH response induced in adult birds was comparable with that in immature chicks. These results demonstrate provocative effects of TRH and hpGRF on GH secretion in the domestic fowl. The sensitivity of the GH response to TRH suggests that it may have a physiological role in the hypothalamic control of GH secretion.

Age Factors↗
PubMed1991

Sexually dimorphic expression of the growth hormone-releasing hormone gene is not mediated by circulating gonadal hormones in the adult rat.

The sexual dimorphism characterizing GH secretion in the rat is thought to be related to differences in the hypothalamic synthesis and release of the GH-regulating peptides, GH-releasing hormone (GHRH), and somatostatin. Therefore, the influence of gender and sex steroid hormones on hypothalamic expression of the GHRH gene in adult rats were examined. GHRH messenger RNA (mRNA) levels were measured in individual rat hypothalami by Northern hybridization analysis using a 32P-labeled complementary DNA encoding rat GHRH. Destruction of hypothalamic GHRH neurons by neonatal treatment with monosodium glutamate caused similar 3-fold reductions in the levels of GHRH mRNA in adult male and female animals. In three separate experiments, hypothalamic GHRH mRNA concentrations in male rats were 2- to 3-fold greater than in randomly cycling females (four or five rats per group; P less than 0.01). In spite of the greater abundance of GHRH mRNA abundance in the male rat hypothalamus, circulating gonadal steroids lacked the ability to modulate GHRH gene expression in adult animals, since neither gonadectomy nor pharmacological sex steroid replacement changed GHRH mRNA levels in the hypothalamus of male and female adult rats. Furthermore, GHRH mRNA concentrations in female rats were similar during the proestrus, estrus, and diestrus phase of the estrous cycle. Also, GH inhibited hypothalamic GHRH gene expression in a sex-specific manner. Exposure to high levels of GH secreted by the MtTW15 tumor for 4 weeks reduced GHRH mRNA concentrations 7-fold in male rats (P less than 0.001) but only 2-fold in females (P less than 0.05). These studies demonstrate that GHRH gene expression in the rat hypothalamus is sexually dimorphic. Basal mRNA levels are greater in male rats, and expression in male hypothalami is more sensitive to feedback inhibition by GH than expression in females. There is no evidence for regulation of GHRH mRNA levels by either testosterone or estrogen in adult rats. These gender differences in GHRH gene expression likely contribute to the generation of a sex-specific pattern of GH secretion.

Animals↗
PubMed1985

Evidence for decreased luteinizing hormone-releasing hormone pulse frequency in men with selective elevations of follicle-stimulating hormone.

To examine the hypothesis that the frequency of endogenous pulsatile LHRH stimulation controls the relative secretion of FSH and LH from the pituitary, we studied men with elevated FSH levels and normal LH levels to determine whether they have an altered frequency of pulsatile LHRH secretion compared to normal men. Because peripheral blood measurements of LHRH do not reflect the pulsatile characteristics of hypothalamic LHRH secretion, and it is generally accepted that the pulse frequency of LH secretion is an index of the frequency of endogenous LHRH pulsation, we used LH pulse frequency as the indicator of LHRH pulse frequency. Frequent blood sampling was performed to characterize LH pulse patterns in five men with selective elevations of FSH and seven age-matched normal men. Beginning at 0800-0930 h, blood samples were obtained every 10 min for 24 h through an indwelling iv catheter. Serum LH and FSH levels were measured by RIA in each sample, and the pattern of LH secretion was determined. Testosterone (T), estradiol, sex hormone-binding globulin, and free T were measured in a pooled serum sample from each man. Men with selective elevations of FSH had fewer LH pulses per 24 h (mean +/- SEM, 10.6 +/- 0.5) than the control group (12.9 +/- 0.6; P less than 0.01). There was no statistically significant difference in LH pulse amplitude (23 +/- 4 vs. 17 +/- 3 ng/ml). There were no statistically significant differences in T (4.9 +/- 0.5 vs. 6.1 +/- 0.5 ng/ml), estradiol (23 +/- 7 vs. 31 +/- 5 pg/ml), sex hormone-binding globulin (7.7 +/- 1.4 vs. 7.7 +/- 1.2 ng bound dihydrotestosterone/ml), or free T (0.16 +/- 0.02 vs. 0.23 +/- 0.04 ng/ml) in these men vs. normal subjects. We conclude that 1) compared to normal men, men with selectively elevated FSH levels have decreased LH pulse frequency, which suggests decreased LHRH pulse frequency; and 2) the relative secretion rates of LH and FSH by the pituitary may be regulated by the frequency of pulsatile LHRH secretion from the hypothalamus.

Adult↗
PubMed1985

Changes in growth hormone (GH) secretion induced by human pancreatic GH releasing hormone-44 in acromegaly: a comparison with thyrotropin-releasing hormone and bromocriptine.

We studied the effects of 100 micrograms human pancreatic GH releasing hormone-44 (GRH) in 35 acromegalic patients. Plasma GH levels significantly increased [basal, 30 +/- 10 (SE) ng/ml; peak, 82 +/- 21 ng/ml; P less than 0.01], but a wide intersubject variability of the responses was found (range, 20-1602%). No relationship was found between the percentage GH increase after GRH and basal values of GH, PRL, or somatomedin-C. All patients also underwent an acute test with bromocriptine (2.5 mg orally) and TRH (200 micrograms iv). When dividing the patients according to their GH responsiveness to bromocriptine (Br), an inverse correlation (r = -0.42, P less than 0.05) was found between percentage of GH changes after GRH and after Br; moreover Br responder patients had a lesser (P less than 0.001) GH increase after GRH (124 +/- 27%) than nonresponders (562 +/- 116%). No relationship was found between the GH response to TRH and GRH, and no differences were found between the percentage GH increase after TRH (513 +/- 117%) and after GRH (349 +/- 71%). We conclude that the tumoral somatotrophs are sensitive to their specific releasing hormone and we suggest that the presence in the adenoma of cells with surface membrane receptors similar to those on the lactotropes may explain the lower sensitivity to GRH of Br responders compared to nonresponders.

Acromegaly↗