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At least 613 records · Page 34Linked to original sources
PubMed2002

Leptin regulates growth hormone-releasing factor, somatostatin, and alpha-melanocyte-stimulating hormone but not neuropeptide Y release in rat hypothalamus in vivo: relation with growth hormone secretion.

It is known that leptin, an adipocyte-derived hormone, exerts a stimulatory effect on growth hormone (GH) secretion in various animal species. However, no previous study examined in vivo whether leptin affects the secretion of GH-releasing factor (GRF), somatostatin (SRIH), and some other closely relevant neurohormones in the hypothalamus. Therefore, in this study we investigated the effects of direct leptin infusion into the hypothalamus on the in vivo release of GRF, SRIH, alpha-melanocyte-stimulating hormone (alpha-MSH), and neuropeptide Y (NPY) in freely moving adult male rats using the push-pull perfusion. Leptin was infused into the median eminence-arcuate nucleus complex at three different concentrations, i.e., 1.0 (normal feeding level), 3.0, and 10 ng/ml (mild obesity level). In normally fed rats, only 10 ng/ml leptin was able to stimulate GH secretion, whereas in 3 d fasted rats, GH release was dose-dependently stimulated by 1.0 and 3.0 ng/ml leptin, although its 10 ng/ml dose did not produce additional effects. The facilitation of GH secretion occurred as increased pulse amplitudes without significant changes in the pulse frequency. During the leptin infusion, the hypothalamic GRF increased and SRIH decreased in magnitudes that approximately paralleled those of GH changes. Leptin stimulated the release of alpha-MSH in the fasted but not fed rats. It is likely that the fasting-induced increase in the hypothalamic alpha-MSH sensitivity to leptin is relevant to ingestive behavior involving leptin. Leptin was without effect on NPY release in either the fed or fasted group. Although it is certain that NPY mediates at least part of the metabolic actions of leptin, NPY is unlikely to be involved in the acute effects of leptin on GH, GRF, and SRIH secretion. These results demonstrate for the first time that leptin can alter the in vivo release of both GRF and SRIH in rat hypothalamus concurrently with the stimulation of GH secretion.

Animals↗
PubMed1975

Follicle-stimulating hormone response to luteinizing-hormone-releasing hormone in patients with hydatidiform mole.

The serum concentration of immunoreactive follicle-stimulating hormone (FSH) and FSH response to synthetic luteinizing-hormone-releasing hormone (LHRH) were investigated in 9 patients with intact hydatidiform moles and 3 patients with aborted moles. The serum concentration of FSH before and after intravenous administration of 200 mug of synthetic LHRH was measured by double antibody radioimmunoassay. Serum FSH was detectable but relatively low compared with the levels seen in the follicular phase of the normal menstrual cycle in all 12 patients. Furthermore, the 12 patients did not respond, or responded subnormally, to exogenously administered LHRH, and there was no significant elevation in serum FSH levels after LHRH injection. The result of the current study is in accord with that of our previous report on the serum concentration of FSH and FSH response to synthetic LHRH during normal pregnancy. Thus, it might be concluded that the follicle-stimulating activity of the anterior pituitary is suppressed by an unknown mechanism during molar pregnancy as well as normal pregnancy.

Adult↗
PubMedDate not supplied

Testosterone effects on luteinizing hormone and follicle-stimulating hormone responses to gonadotropin-releasing hormone in the mouse.

Studies in the mouse have demonstrated for the first time in vivo regulation of gonadotropin-releasing hormone (GnRH) on the minute-to-minute dynamics of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) release and the effects of testosterone on this regulation. Intact and castrated mice with different testosterone levels (3-9 ng/mL) were challenged with exogenous GnRH while under general anesthesia to block endogenous GnRH release. Plasma concentrations of LH and FSH were determined by radioimmunoassay from sequential blood samples collected from anesthetized mice with in-dwelling catheters. The release of LH was correlated with the infusion of different doses of GnRH (0.35, 3.5, and 35 ng) in both intact and castrated mice (r = 0.942, approximately 0.999). GnRH-stimulated LH release was significantly lower in intact mice and in castrated mice with high testosterone levels than in castrated mice with low testosterone levels (P < .05). However, GnRH did not induce FSH release except in castrated males with low testosterone levels and at the highest dose of GnRH. The profiles of FSH release in intact mice and castrated mice with the highest testosterone levels were significant lower than the other groups (P < .05). In conclusion, release of LH, but not FSH, was correlated with increasing dosages of GnRH (r = 0.970), and testosterone significantly suppressed GnRH-stimulated LH release in the mouse (P < .05).

Animals↗
PubMed1989

Suppression of bioactive and immunoreactive follicle-stimulating hormone and luteinizing hormone levels by a potent gonadotropin-releasing hormone antagonist: pharmacodynamic studies.

Dose-dependent gonadotropin suppression by a potent gonadotropin-releasing hormone (GnRH) antagonist, Nal1 Glu6 [( Ac-D2Nal1,D4ClPhe2,D3Pal3,Arg5,DGlu(AA)6,- DAla10]GnRH), was determined in five postmenopausal women by frequent sampling for immunoreactive luteinizing hormone (I-LH) and immunoreactive follicle stimulating hormone (I-FSH) for 72 hours after single intramuscular (IM) injections of 10, 50, 150, and 300 micrograms/kg. Bioactive (B) LH and B-FSH also were measured after the IM administration of the 50-micrograms/kg dose. Serum levels of Nal1 Glu6 were determined by a radioreceptor assay for the first 24 hours after the 50-micrograms/kg IM dose and in three women after a 10-micrograms/kg intravenous (IV) dose. While the disappearance rate of serum Nal1 Glu6 after a 10-micrograms/kg IV injection was rapid, gonadotropin suppression persisted longer than detectable serum levels. In contrast, after a 50-micrograms/kg IM injection, the decline from peak circulating levels was slower, contributing to its longer duration of action (greater than 24 hours). All IM doses tested resulted in a similar 51% to 63% decrease in I-LH, which was maximal by 8 hours. The duration of action was dose-dependent, with decreased levels lasting up to 72 hours at the 300-micrograms/kg dose. While decline of I-FSH was smaller (14% to 33%), the duration of suppression was also dose-dependent, although the nadir occurs later (8 to 9 hours after administration) and suppression lasted longer (72 hours at the 150-micrograms/kg dose). The reduction of B-LH was greater than that of I-LH and the suppression of B-FSH also was greater than that of I-FSH.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1986

Increased frequency of pulsatile luteinizing hormone-releasing hormone administration selectively decreases follicle-stimulating hormone levels in men with idiopathic azoospermia.

Men with idiopathic azoo-oligospermia and selective elevations of follicle-stimulating hormone (FSH) levels have evidence for decreased luteinizing hormone-releasing hormone (LH-RH) pulse frequency. We assessed whether increasing the frequency of pulsatile LH-RH stimulation can lower FSH levels in such men. We administered 5.0 microgram of pulsatile LH-RH subcutaneously at intervals of 30, 60, and 120 minutes for 1 week to four men who had azoospermia, elevated FSH levels, and normal LH and testosterone (T) levels. The order of administration was varied among subjects. Frequent blood samples were obtained for 6 hours before LH-RH treatment and during the last 6 hours of each regimen. Before LH-RH treatment, the FSH levels (mean +/- standard error of the mean) were 359 +/- 18 ng/ml (normal range, 30 to 230 ng/ml). During LH-RH treatment, FSH levels progressively declined from 397 +/- 68 ng/ml to 237 +/- 70 ng/ml to 175 +/- 43 ng/ml as the frequency of administration increased from every 120 to 60 to 30 minutes, respectively (P less than 0.05). Unlike the FSH levels, which showed a progressive decline, LH, T, and estradiol levels showed no consistent relationship to LH-RH pulse frequency. We conclude that (1) in men with idiopathic azoospermia and elevated FSH levels, it is possible to decrease FSH levels by increasing the frequency of pulsatile LH-RH stimulation; (2) this decline does not appear to be a result of changes in steroid feedback or pituitary down-regulation; and (3) the frequency of pulsatile LH-RH stimulation can differentially modulate LH and FSH secretion by the pituitary gland.

Adult↗
PubMed1993

Response to gonadotrophin-releasing hormone by the intact male dog: serum testosterone, luteinizing hormone and follicle-stimulating hormone.

In Expt 1, gonadotropin-releasing hormone (GnRH) (Cystorelin, CEVA) was administered intramuscularly to two intact male dogs; one dog received one injection of 50 micrograms GnRH and one dog received four daily injections of 50 micrograms GnRH. Both dogs exhibited a significant and immediate rise in luteinizing hormone (LH) following GnRH administration, with a peak observed at 15 min following injection. Testosterone was increased over baseline concentrations for 5 and 7 days, respectively, after the injection. In Expt 2, eight intact male dogs were injected intramuscularly with 0.7 microgram GnRH (Factrel, Fort Dodge) kg-1. Baseline testosterone concentrations were established by daily sampling for 14 days before treatment. All dogs exhibited an LH peak 15 min and a testosterone peak 60 min after the GnRH injection. Testosterone concentrations had returned to baseline concentrations by 4 h after the injection. Testosterone tended to fall below baseline concentrations for several days following the injection of GnRH. No peak was noted for follicle-stimulating hormone. In Expt 3, five additional dogs were injected with 0.7 microgram GnRH (Factrel, Fort Dodge) kg-1. Testosterone concentrations rose in all dogs 1 h after the injection and returned to baseline concentrations by 24 h after injection. In the male dog, GnRH stimulated an LH peak 15 min and a testosterone peak 1 h after injection. Further investigations are needed to elucidate the different effects on testosterone concentration observed with two different GnRH preparations.

Animals↗
PubMed1993

Recombinant human erythropoietin (rhEPO) treatment potentiates growth hormone (GH) response to growth hormone releasing hormone (GHRH) stimulation in hemodialysis patients.

On the basis of previously described effects of recombinant human erythropoietin (rhEPO) treatment on endocrine abnormalities present in uremia, we assessed the possible effect of treatment with rhEPO on growth hormone (GH) response to growth hormone releasing hormone (GHRH) in a group of uremic patients. Eight patients on maintenance hemodialysis for 12 to 228 months, not previously treated with rhEPO, were tested with 100 micrograms of GHRH i.v. in bolus before and after three months of rhEPO treatment (40 U/kg i.v. three times a week). Before treatment, the GH response to GHRH was characterized, in uremic patients, by remarkable differences in plasma GH values and in the pattern of response curve in single patients. The variability of GH response was not modified after rhEPO treatment; however, an overall potentiation of GH response with a significant increase of plasma GH (p = 0.017 at 15 min, p = 0.035 at 30 min after GHRH injection) was observed in the tests performed after treatment. rhEPO administration induced an evident improvement of anemia, blood hemoglobin concentration being 5.3-7.6 g/dl before and 9.1-11.3 g/dl after treatment; however a demonstrable correlation between the potentiation of GH response to GHRH and the increase of hemoglobin concentration was not observed.

Anemia↗
PubMed1996

Effect of growth hormone releasing hormone on growth hormone, prostaglandin E2 and insulin in non-insulin-dependent diabetic patients.

In a previous paper we demonstrated a link between growth hormone releasing hormone (GHRH) and prostaglandin E2 (PGE2) in their action on growth hormone (GH) in normal subjects. However, in diabetes mellitus various disturbances of GH and PGE2 secretion have been reported. In the present study the response of GH, PGE2 and insulin to GHRH (1 microgram/kg b.w.) intravenously was investigated in 12 poorly controlled non-insulin-dependent diabetic patients (8 males and 4 females) and 10 normal volunteers (5 males and 5 females). After GHRH injection, GH increased in diabetic patients from 2.28 +/- 0.52 mU/l to 14.76 +/- 1.29 mU/l at 30 min (p < 0.001). This response was not statistically different compared to the control subjects. The basal values of plasma PGE2 were significantly lower in diabetic patients than in control subjects. GHRH induced a slight but significant increase of PGE2 in normal subjects (9.80 +/- 0.44 pg/ml at 0 min; 14.50 +/- 1.30 pg/ml at 90 min, p < 0.05) and did not have any effect on PGE2 in diabetic patients. Serum insulin decreased significantly after GHRH in both normal subjects and diabetic patients at 60 min. We conclude that GH response to GHRH is not significantly impaired in poorly controlled non-insulin-dependent diabetic patients. The lack of an effect of GHRH on PGE2 in diabetic subjects provides further evidence of abnormal PGE2 synthesis or metabolism in this disorder. The physiological significance of the GHRH suppressive effect on serum insulin remains to be explained.

Adult↗
PubMed1997

Effects of sumatriptan on growth hormone releasing hormone-stimulated growth hormone secretion in acromegaly.

Sumatriptan (SU), a specific 5-HT1D receptor agonist, was recently shown to be able to increase growth hormone (GH) levels in normals, but not in acromegalics, while no effect was seen on prolactine (PRL). SU is also able to produce an increase in GH response to growth hormone releasing hormone (GHRH) in prepubertal children. In this study we investigated whether SU administration influences GHRH-induced GH secretion in 8 acromegalics, and 6 age-matched normal volunteers, as a control group. We evaluated the effects of SU (6 mg s.c.) or placebo (PL) administration on GHRH (1 microgram/kg bw i.v.)-induced GH and PRL secretion. After SU priming the GH response to GHRH did not changed in acromegalics, but significantly decreased in controls, in comparison with that observed after PL plus GHRH. In acromegalics, no difference in GH peak was seen after SU plus GHRH and PL plus GHRH, nor was any difference seen in AUC between tests. In controls, no difference was seen in GH peaks, while SU priming significantly (P < 0.03) decreased the AUC 90-120 min of GH after GHRH administration. In acromegalics, SU did not change the slight GHRH-induced increase in PRL levels. Our study documents that 5-HT1 D receptors do not interfere with GHRH-stimulated GH secretion in acromegalic subjects. In normals, SU is able to decrease GH response to GHRH, thus confirming that 5-HT1D receptors are able to modulate GH secretion in normals.

Acromegaly↗
PubMed1983

Uptake and retention of moulting hormones by the integument of crayfishes in vitro: I. Influence of temperature, hormone concentration and hormone structure.

Uptake kinetics of [3H]ecdysone into crayfish hypodermis in vitro reveals three different components: a very rapid (within 1 min), highly temperature-dependent (Q10 = 3) and high uptake rate, a second much lower uptake which is only slightly temperature-dependent (Q10 = 1-1.3), and a plateau which is reached after about 20 min at 20 degrees C. Preincubation of tissue with unlabelled hormone reduces the initial uptake rate to a value characteristic for the second, less steep uptake phase. The activation energy for the initial uptake is 45 kJ/mole. At equilibrium the hormone is 4-fold enriched as compared to the medium, the delta G for this enrichment being 3 kJ/mole. The efflux is much lower than the influx and is linear. There is no linear relation between external hormone concentration and initial uptake rate. The initial uptake can be significantly reduced by an excess of diverse ecdysteroids with moulting hormone activity but not by hydrocortisone.

Animals↗
PubMed2000

Effects of growth hormone (GH) and growth hormone releasing hormone (GHRH) on progesterone and estradiol release from cultured rat granulosa cells.

OBJECTIVES: It has been reported that GHRH-GH-IGF-1 system plays an important role in the regulation of ovarian follicular development and maturation. METHODS: In order to evaluate the direct effects of growth hormone releasing hormone (GHRH) and growth hormone (GH) on steroidogenesis, the effects of GHRH and GH on progesterone and estradiol release from cultured rat granulosa cells were examined. The progesterone and estradiol in supernatants were measured with RIA methods. RESULTS: Our results demonstrated that the addition of GH to the culture medium produced a marked stimulation of progesterone and estradiol. The stimulating effects were observed after administration of GH in all concentrations: 1, 10, 100 nM during 60 and 120 mins of incubation. During 240 mins of incubation the minimal stimulation of progesterone and estradiol was found. However, GHRH administered in 1, 10 and 100 nM did not change progesterone and estradiol release from cultured granulosa cells. CONCLUSION: Growth hormone (GH) but not GHRH has direct stimulating effects on progesterone release from cultured rat granulosa cells.

Journal Article↗
PubMedDate not supplied

Pseudohypoparathyroidism type Ia and growth hormone deficiency. Growth hormone releasing hormone receptor defect?

We report a boy with pseudohypoparathyroidism (PHP), hypothyroidism and low growth hormone (GH) values with no response to growth hormone releasing hormone (GHRH). He presented at age 17 mo because of developmental delay. He had the typical features (short stature, obesity, round face, brachydactyly) of Albright's hereditary osteodystrophy (AHO) and the biochemical profile of PHP; low serum calcium and high phosphate, raised parathormone (PTH) values and lack of response of urinary phosphate and cyclic AMP to PTH administration. The serum total thyroxine value (T4) was 37.32 nmol/L and the thyroid stimulating hormone (TSH) 29 mU/L. Peak GH values during two provocative tests (Glucagon, L-Dopa) were <2.5 microg/L and <1.7 microg/L, respectively, while following GHRH administration the maximum GH value was 0.2 microg/L. The IGFI value was 65 ng/ml and rose to 253 ng/ml after GH administration for three days. This boy had PTH and TSH receptor defect and we speculate that he also has GHRH receptor defect.

Journal Article↗
PubMed2004

Phenotypic analysis and growth response to different growth hormone treatment schedules in two siblings with an inactivating mutation in the growth hormone-releasing hormone receptor gene.

Mutations in the GHRH receptor (GHRHR) gene (GHRHR) are emerging as a common cause of familial isolated growth hormone deficiency (IGHD) type IB. The use of gonadotropin-releasing hormone (GnRH) analogues has been advocated as a tool to delay puberty in patients with isolated GH deficiency (IGHD), allowing longer time for the beneficial effect of exogenous human GH (hGH) treatment on growth. We describe two male siblings with IGHD due to a homozygous missense GHRHR mutation who, because they were started on hGH therapy at different ages, presented with different height SDS at the onset of puberty and therefore had different predicted target heights. The shorter brother was treated with GnRH analogue plus hGH for 3 years, whereas the other brother received only hGH. Despite different predicted heights at the onset of puberty, they attained similar final heights. We conclude that in patients with IGHD, GnRH analogue treatment should be considered to delay puberty and obtain a maximal growth response if hGH treatment is started in late childhood and the predicted height at puberty onset is below the genetic target.

Adolescent↗
PubMed1987

Renewal timing of long-acting depot luteinizing hormone-releasing hormone agonist (Zoladex) is critical in the treatment of hormone-dependent rat prostatic carcinoma (R3327-H).

The effects of luteinizing hormone-releasing hormone (LHRH) agonist (Zoladex) treatment on hormone-dependent rat prostate adenocarcinoma (R3327-H) were investigated based on changes in tumor volume and histology. Tumor-bearing rats were treated for 10 weeks with Zoladex in depot preparation by implantation every 2, 4, or 6 weeks. Tumor growth rate was similar in the castrated group and in the rats treated every 2 weeks with Zoladex. This growth rate was significantly slower than in animals treated with Zoladex every 6 weeks and the nontreated group. The growth rate in rats treated every 4 weeks appeared to be faster than that in the castrated animals (not significant). Changes in testosterone levels measured during Zoladex treatment correlated with tumor growth kinetics. Zoladex implantation yields effective and complete androgen deprivation only in the rats with two weekly depot renewal regimen. Tumor histology indicated that the stromal as well as the glandular epithelial cells responded to both castration and to Zoladex treatment. However, in tumors from rats treated with Zoladex every 4 and 6 weeks progressive increasing signs of restoration of normal elements, comparable to non-treated tumors were observed. These results strongly suggest that careful attention has to be paid to the timing of LHRH depot renewal in prostate cancer treatment.

Androgens↗
PubMed1991

Hypothalamic luteinizing hormone-releasing hormone content and serum luteinizing hormone levels in male rats during wallerian degeneration of sympathetic nerve terminals after superior cervical ganglionectomy.

The main hypothesis of this study was that sympathetic neurons located at the superior cervical ganglia (SCG) control luteinizing hormone (LH) releasing mechanisms by acting at a hypothalamic site. To test this, medial basal hypothalamus (MBH) luteinizing hormone-releasing hormone (LHRH) content and serum LH levels were measured in male rats subjected to superior cervical ganglionectomy (SCGx) or sham-operation 14 or 38 h earlier, at the time of degeneration of nerve endings post-SCGx. Significantly augmented MBH LHRH levels and decreased circulating LH were found in SCGx rats. In animals subjected to SCGx 14 h earlier and receiving a single injection of the alpha 1-adrenergic blocker prazosin, the beta-adrenergic blocker propranolol or a mixture of both drugs 45 min before sacrifice, only the injection of prazosin prevented the decrease of plasma LH levels. Neither treatment prevented the increase in MBH LHRH content. When prazosin was given every hour starting from the 10th to the 13th h after surgery, it was effective to prevent both the increase of MBH LHRH content and the decrease of serum LH found during sympathetic nerve degeneration. Similar repetitive injections of propranolol resulted in the greatest depression of serum LH, and in the greatest increase of MBH LHRH observed. Serum LH response to LHRH injection was similar in SCGx and sham-operated rats. The data indicate that SCG neurons exert, through inhibitory alpha 1-, and weaker, stimulatory beta-adrenoceptors, a significant influence on LHRH release at a supra-hypophysial site.

Animals↗
PubMed1983

Combined testing of anterior pituitary gland with insulin, thyrotropin-releasing hormone, and luteinizing hormone-releasing hormone.

Provocative tests of hypothalamic-pituitary function were performed in 20 healthy subjects to learn whether the simultaneous testing by three agents--insulin, thyrotropin-releasing hormone, and luteinizing hormone-releasing hormone--was feasible. The responses to simultaneous testing on one day did not differ significantly from those to testing on three separate days. The time and expense of pituitary-hypothalamic testing can thus be much reduced with no impairment of reliability and with no increased risk to the patient.

Adult↗
PubMed1979

Enzymes involved in the degradation of thyrotropin releasing hormone (TRH) and luteinizing hormone releasing hormone (LH-RH) in bovine brain.

As part of an investigation of neuropeptide inactivation mechanisms, we have resolved an enzymatic activity in bovine brain which catalyzes the deamidation of thyrotropin releasing hormone (TRH) and the hydrolysis of the Pro9--Gly10--NH2 bond of luteinizing hormone releasing hormone (LH-RH) from a second LH-RH degrading activity which does not degrade TRH. The former activity is similar, if not identical to, the post-proline cleaving enzyme in kidney as it is active toward the post-proline cleaving enzyme substrate CbzGly--Pro--Leu--Gly and inhibited by CbzPro--Phe and diisopropylfluorophosphate. In addition, products derived from the degradation of TRH and LH-RH by this activity show a specific cleavage on the carboxyl side of a proline residue. The latter activity has not yet been characterized with respect to its site of cleavage of the LH-RH molecule due to the presence of other contaminating peptidases.

Amino Acid Sequence↗
PubMed1988

Binding of growth hormone-releasing hormones and enkephalin-derived growth hormone-releasing peptides to mu and delta opioid receptors in forebrain of rat.

The purpose of this study was to compare the binding potency to opioid receptors of met-enkephalin-derived, hypophysiotrophic peptides with their reported growth hormone (GH)-releasing strengths in vitro and further, to determine the relative selectivity of each peptide for mu and delta opioid binding sites in the forebrain of the rat. A series of (GH)-releasing pentapeptides and hexapeptides (GHRP's), as well as rat (rGHRH) and human (hGHRH) growth hormone-releasing hormones were tested for preferential binding to specific opioid receptors. The site selectivity of each peptide was determined by its ability to compete for binding with synthetic ligands for mu (Tyr-D-Ala-Gly-MePhe-Gly-ol; DAGO) and delta ([D-Pen2,5]-enkephalin; DPDPE) opioid receptors. The various peptides differed in their selectivities for the two opioid receptors in that most of the GHRP's were mu-selective, while the naturally occurring GHRH's were delta-selective. Amidation of the C-terminal decreased delta selectivity. Besides affecting selectivity for the site, structural changes that enhanced GH-release by enkephalin-derived peptides also decreased their potency to compete for opioid binding sites. For example, dose-response curves for His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 (SK&F 110679) inhibition of the binding of DAGO and DPDPE yielded IC50's of 6 and 20 microM, respectively. In contrast, Tyr-D-Trp-Gly-Phe-Met-NH2 (BI360), which is 1 X 10(3) times weaker than SK&F 110679 in releasing GH, had IC50's of 0.1 microM and 0.08 microM for inhibition of the binding of DAGO and DPDPE, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗