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PubMed1991

Effect of estrogen administration on endogenous and luteinizing hormone-releasing-hormone-induced luteinizing hormone secretion and follicular development in the lactating sow.

The objectives of this study were to investigate whether estradiol treatment during lactation modifies 1) the patterns of endogenous LH, FSH, and prolactin (PRL) release; 2) the sensitivity of the pituitary to exogenous injections of LHRH; and 3) the responsiveness of the ovarian follicles to gonadotropin. Plasma LH, FSH, and PRL were determined in samples taken repeatedly from 18 sows on Days 24-27 of lactation. Ovaries were then recovered, and follicular development was assessed by measuring the follicular diameter (FFD) and follicular fluid estradiol-17 beta concentration (FFE) of the ten largest follicles dissected from each ovary. Sows were randomly allocated to one of four treatments: 1) Group C (4 sows) received no treatment; 2) Group LHRH (5 sows) received 800 ng of LHRH every 2 h throughout the sampling period; 3) Group E2 (4 sows) received subcutaneous implants containing estradiol-17 beta 24 h after start of sampling; 4) Group LHRH + E2 (5 sows) were administered a combination of LHRH and estradiol-17 beta implants. Between-animal variability for plasma LH, FSH, and PRL was considerable. LH concentration and LH pulse frequency increased (p less than 0.05) after LHRH treatment in the LHRH and LHRH + E2 groups; however, an acute inhibition of LH secretion was observed in the latter group immediately after estradiol implant application. In the absence of LHRH treatment, estradiol caused chronic inhibition of LH secretion. Follicular development was greater in the LHRH and LHRH + E2 groups compared to the C and E2 groups (p less than 0.05 for both FFD and FFE).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Luteinizing hormone (LH) and corticosterone in proestrous afternoon restore the follicle-stimulating hormone secretion at early estrus in adrenalectomized LH-releasing hormone antagonist-treated rats.

Administration of the antiprogestagen RU486 in the morning of proestrus abolishes the secondary surge of FSH during early estrus in the rat without preventing the drop in serum inhibin. In addition, the injection of an ovulatory dose of LH to RU486-injected rats does not restore the secondary surge of FSH. Since RU486 is a potent antiprogesterone with antiglucocorticoid activity, in the first experiment we compared the effects of RU486 and a specific antiprogesterone serum (APS), administered on proestrus, on the secretion of FSH during early estrus. While RU486 and APS reduced the primary surge of LH and FSH, only RU486 abolished the secondary secretion of FSH. In the second experiment, rats injected with LHRH antagonist (LHRHa) and ovine LH (oLH) were adrenalectomized (ADX) or sham-ADX in the morning and injected with corticosterone (B) or oil in the afternoon of proestrus. LHRHa completely eliminated, and oLH restored, the secretion of FSH at 0200 h in estrus. ADX reduced FSH serum concentration at 0200 h in estrus, and B reversed this effect in rats injected with LHRHa and oLH. The results of these experiments indicate that, in the rat, the LHRH-independent secretion of FSH during early estrus is evoked by the combined effects of the preovulatory surge of LH and the rise in serum B on proestrous afternoon.

Adrenal Glands↗
PubMed1995

Effects of indirect selection for pituitary responsiveness to gonadotropin-releasing hormone on the storage and release of luteinizing hormone and follicle-stimulating hormone in prepubertal male lambs.

Divergent selection based on the LH response to a 5-micrograms dose of GnRH in 10-wk-old Finn Dorset ram lambs has created two lines of sheep that differ significantly in their response to both physiological and pharmacological dosages of GnRH. The aims of this study were to investigate whether there are between-line differences in endogenous LH and FSH secretion in ram lambs, as in the adult ewes, and to determine whether these differences are related to differences in storage of gonadotropins within the pituitary glands of the two lines. To address the first aim, endogenous LH and FSH secretion was monitored in 20 ram lambs from each line for a 6-h period at 2, 6, and 10 wk of age. To investigate potential between-line differences in gonadotropin storage, the LH responses to two acute challenges with either 0.5, 5.0, or 50.0 micrograms of GnRH were examined in 10-wk-old ram lambs from each line. The results demonstrated that the between-line difference in the LH response to a 5-micrograms GnRH challenge in ram lambs is accompanied by significant between-line differences in the regulation of endogenous gonadotropin secretion. Specifically, lambs from the High line secreted LH pulses of significantly greater amplitude than did lambs from the low line at 2 and 10 wk of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1998

Involvement of estrogen and follicle-stimulating hormone on basal and luteinizing hormone (LH)-releasing hormone-stimulated LH secretion in RU-486-induced 3-day estrous cycle in the rat.

Administration of 4 mg of the antiprogestogen RU-486 on proestrus (Day 1) to 4-day-cyclic rats advances the pituitary desensitization to negative estrogen feedback and enhances pituitary responsiveness to LHRH. These effects of RU-486 lead to a 1-day estrous cycle shortening. Moreover, administration of RU-486 in this study increased serum estradiol-17beta and decreased FSH concentrations during diestrus (experiment 1). The aim of the study was to examine the contribution of the excess of estrogen and the deficiency of FSH during diestrus to the 1-day estrous cycle-shortening effect of RU-486 when injected on Day 1 in 4-day-cyclic rats. The aim of the second and third experiments was to evaluate the effects of 3 mg/0.2 ml oil of the antiestrogen LY117018-HCl (LY) at 1800 h on Days 2 and 3, or 10 IU/0.2 ml saline of a recombinant human FSH (rhFSH) at 1700 h on Day 3 and at 0900 h on Day 4, with or without 100 ng/0.5 ml saline of LHRH at 1200 h on Day 4, on uterine weight and serum concentrations of LH and estradiol-17beta at 1300 h on Day 4 in rats given oil or RU-486 on Day 1 or 2. The aim of the fourth experiment was to evaluate the effect of combined LY and rhFSH treatments on uterine weight and serum levels of LH and estradiol-17beta in rats injected with RU-486 on Day 1. Administration of RU-486 on Day 1 significantly increased serum estradiol-17beta on Days 3 and 4, whereas administration on Day 2 slightly increased serum estradiol-17beta on Day 4 only. Injection of RU-486 on either Day 1 or 2 decreased FSH serum concentrations on Days 3 and 4 to a similar extent. Treatment with LY reduced both basal and LHRH-stimulated LH secretion only in rats injected with RU-486 on Day 1, while rhFSH treatment attenuated basal and stimulated LH secretion regardless of treatment. Treatment with LY and rhFSH combined completely reversed the effects of RU-486 on Day 1 on LH serum concentrations. These data suggest that both the increased estradiol-17beta and the decreased FSH serum concentrations during diestrus in rats given RU-486 on proestrus are involved in the changes of pituitary function leading to a 1-day estrous cycle shortening.

Animals↗
PubMed1979

The effect of repeated intramuscular gonadotrophin-releasing hormone injections on luteinizing hormone, follicle-stimulating hormone, testosterone, oestrogens, dehydroepiandrosterone and dehydroepiandrosterone sulfate in normal men.

The endocrine response to three daily intramuscular injections of 500 microgram LH-RH was measured in 9 normal men during a period of 3 days. A marked but declining response in LH was seen in addition to a significant increase in the serum concentration of FSH, testosterone, oestradiol and the urinary excretion of oestrogenic substances. No change could be demonstrated in the DHA, DHAS or cortisol secretion which confirms our previous results of a direct effect of clomiphene on adrenal steroidogenesis.

Adrenal Cortex↗
PubMed1986

Continuous infusion of growth hormone releasing hormone does not alter the growth hormone response to different stress stimuli.

Continuous infusion of GHRH, as well as a bolus injection of GHRH, specifically stimulates the release of GH by the anterior pituitary. However, repetitive bolus injections of GHRH result in diminished responses of GH, while a constant infusion of GHRH cannot maintain high serum GH levels. To investigate whether different GH-releasing stimuli are able further to challenge the somatotroph being exposed to continuous infusion of GHRH, we determined the GH response to insulin-induced hypoglycaemia and bicycle exercise. Six normal volunteers received a bolus of 50 micrograms GHRH or vehicle followed by a continuous infusions of GHRH 1-29 amide (1 microgram/kg/h) or vehicle for 2.5 h. GHRH bolus and infusion resulted in elevated GH levels, but GH levels fell to values not significantly different from baseline levels after 150 min, GH plasma levels rose again, however, in response to insulin hypoglycaemia and bicycle exercise after both GHRH or vehicle infusion. Thus, the somatotroph's responsiveness to GHRH remains intact to respond to stress stimuli after continuous GHRH infusion.

Adult↗
PubMed1987

Growth hormone and prolactin secretion after growth hormone-releasing hormone administration, in anorexia nervosa patients, normal controls and tamoxifen-pretreated volunteers.

Anorexia nervosa is associated with several abnormalities in GH secretion elicited by different stimuli. To investigate the precise mechanism of this alteration, GHRH was administered to 14 women: a group of eight anorexia nervosa patients in the acute phase of their illness and a control group of six age-matched volunteers. As patients with anorexia nervosa have chronic low oestrogen values, the volunteer women of the control group underwent a second GHRH test after pretreatment with the oestrogen receptor blocker tamoxifen. GHRH 1-29 (1 microgram/kg i.v.) induced a GH peak (mean +/- SEM) of 28.2 +/- 5.1 ng/ml (GH ng/ml x 2 = mU/l) at 30 min in the anorectic patients. This value was no different from the GHRH-stimulated GH peak in the control women (28.1 +/- 10.0 ng/ml). Tamoxifen pretreated women had a GH peak after GHRH of 35.6 +/- 9.7 ng/ml, not significant versus control test. Compared with the control group, oestrogen levels were significantly lower in anorectic patients and higher in tamoxifen-treated women. GHRH administration induced a small PRL peak at 15 min that was similar in the three groups tested. After this 15 min peak, PRL in both anorexic and tamoxifen-treated women returned toward basal values steadily. However, in untreated control women a second PRL peak was evident at 60 min. In conclusion, GHRH-induced GH secretion in anorexia nervosa patients was similar to that in control subjects and in controls under oestrogen receptor blockade.

Acute Disease↗
PubMed1989

Intrasellar gangliocytoma containing gastrin and growth hormone-releasing hormone associated with a growth hormone-secreting pituitary adenoma.

A 74-year-old acromegalic found to have an intrasellar gangliocytocytoma and GH-secreting pituitary adenoma is described. The gangliocytoma contained immunoreactive gastrin and, to a lesser extent, GHRH, and the adenoma immunostained for GH. Gastrin has not been previously reported in hypothalamic gangliocytomas. Since this peptide has been demonstrated in normal hypothalamus and pituitary, and provokes GH release when administered intraventricularly, it may have caused GHRH release from the gangliocytoma by a local paracrine action and led to adenoma formation and acromegaly.

Adenoma↗
PubMed1990

The interaction between clonidine and growth hormone releasing hormone in the stimulation of growth hormone secretion in man.

Six normal adult males were given clonidine and GHRH either separately, or in combination, in random order. The peak serum GH concentrations elicited by clonidine or GHRH were variable but one factor influencing the GH response to GHRH was the GH secretory status in the hour prior to the administration of the GHRH. Peak serum GH concentrations attained were significantly greater when serum GH concentrations were rising (mean 52.9 mU/l, SD 17.2) than if they were falling (mean 27.5 mU/l, SD 13.3) or unchanged/undetectable (mean 20.6 mU/l, SD 9.8) (one-way ANOVA, F = 8.77; P = 0.004). The GH response to clonidine was not influenced by the secretory status in the hour prior to administration of clonidine. Pretreatment with clonidine did not augment the peak serum GH response to GHRH but the direction of response was more predictable than when GHRH was administered separately or repeatedly. Prior treatment with GHRH(1-29)-NH2 led to a marked attenuation of the peak serum GH response to clonidine. These results suggest that the alpha-2 adrenergic agonists probably stimulate GH secretion through pathways other than just GHRH.

Adult↗
PubMed1992

Galanin reinstates the growth hormone response to repeated growth hormone-releasing hormone administration in man.

OBJECTIVE: To clarify the mechanism by which galanin, a 29-amino-acid peptide, increases GH secretion in man. DESIGN: We studied the GH-releasing effect of this neurohormone (galanin, 15 micrograms/kg) infused over 60 minutes after 120 minutes of saline, following a previous GHRH bolus (GHRH 1 microgram/kg i.v. at 0 minutes, galanin infused from 120 to 180 minutes) and coadministered with the second of two consecutive GHRH boluses (GHRH every 120 minutes, galanin infused from 120 to 180 minutes). PATIENTS: Fourteen healthy male subjects, aged 20-34 years, in two groups (group A, 20-31 years (n = 8); group B, 25-34 years (n = 6)) were studied. MEASUREMENT: Blood samples were drawn every 15 minutes of 255 minutes. Serum GH was measured in duplicate by IRMA. Statistical analysis of the data was carried out by non-parametric ANOVA test. RESULTS: The GH response to galanin infused 120 minutes after saline overlapped with that induced by the neuropeptide infused following previous GHRH bolus (AUC, mean +/- SEM: 317.3 +/- 73.2 vs 326.8 +/- 54.2 micrograms/l/h). The GH-releasing effect of the second GHRH bolus (126.9 +/- 32.3 micrograms/l/h) was lower than that of the first one (503.4 +/- 41.3 micrograms/l/h; P = 0.0002). Galanin markedly enhanced the GH responses to the second GHRH bolus (1118.0 +/- 212.7 micrograms/l/h; P = 0.0002 vs second GHRH bolus alone) so that it did not significantly differ from the first one (710.9 +/- 107.8 micrograms/l/h). CONCLUSIONS: Our results show that the GH-releasing effect of galanin is not modified by GHRH pretreatment and that the neuropeptide reinstates the GH response to the repeated GHRH stimulation in man. They suggest that these effects are due to the inhibition of hypothalamic somatostatin release.

Adult↗
PubMed1992

Differential effects of arginine on growth hormone releasing hormone and insulin induced growth hormone secretion.

OBJECTIVE: We wished to investigate the interaction of arginine, GHRH and insulin stress on GH secretion. DESIGN: Six healthy, non-obese volunteers underwent seven separate studes in random order. They received (1) insulin alone at 0 minutes; (2) GHRH alone at 15 minutes; (3) arginine alone at 0-30 minutes; (4) arginine at 0-30 minutes and GHRH at 15 minutes; (5) insulin at 0 minutes and arginine at 0-30 minutes; (6) insulin at 0 minutes, GHRH at 15 minutes and arginine at 0-30 minutes; (7) insulin at 0 minutes and GHRH at 15 minutes. MEASUREMENTS: GH and PRL were measured from -30 to 150 minutes at intervals of 15 minutes. RESULTS: Arginine increased GH responses to GHRH and decreased GH responses to hypoglycaemia, but this inhibitory effect of arginine was reversed by GHRH. CONCLUSIONS: The findings suggest that arginine-induced GH release is mainly mediated by a decrease in somatostatinergic tone, while GH responses to insulin stress are probably mediated by both an increase in hypothalamic GHRH release and inhibition of somatostatin.

Adult↗
PubMed1993

Protein intake during aggressive calorie restriction in obesity determines growth hormone response to growth hormone-releasing hormone after weight loss.

OBJECTIVE: We evaluated the influence of two types of calorie restriction, total fast or very low calorie diet, on GH responsiveness to GHRH in severely obese patients. DESIGN: Twenty patients with massive obesity underwent one of two types of calorie restriction, total fast (10 patients) or very low calorie diet (10 patients). MEASUREMENTS: Fasting GH, IGF-I, glucose, insulin and GH secretion after GHRH (100 ug i.v.) were assessed in all patients before and after diet therapy. RESULTS: Both types of diet produced similar weight reduction (total fast, 5.6 +/- 1.6 kg/m2 vs very low calorie diet, 5.6 +/- 1.5 kg/m2 mean +/- SD). A significant increase in the integrated GH secretion was observed after weight loss with very low calorie diet (17 +/- 9 vs 27 +/- 12 mU/l min; P < 0.05). However, no change was found in GH response after weight loss with total fast (13 +/- 5 vs 15 +/- 7 mU/l min). Glucose, insulin and IGF-I levels showed a significant decrease with weight reduction which was similar for both groups. CONCLUSION: These findings suggest that the type of dietary manipulation during calorie restriction in obese patients may influence the changes in GH response to GHRH after weight loss.

Adult↗
PubMed1995

Induction of cellular follicle-stimulating hormone in the hamster adenohypophysis requires intermittent stimulation by luteinizing hormone releasing hormone.

We investigated the effectiveness of continuous vs intermittent LHRH stimulation of the neonatal female anterior pituitary gland on inducing cellular FSH immunoreactivity in the Golden Syrian hamster. Neonatal female pituitary glands were grafted beneath the right renal capsules of hypophysectomized-ovariectomized adult hosts with a catheter implanted in the external jugular vein. In experiment 1, vehicle or LHRH (6 ng/h) was infused continuously or LHRH was pulsed at 1 h (6 ng) or 12 h (72 ng) intervals through the catheters for 8 days. Hamsters were decapitated for collection of trunk blood shortly after the end of treatment, and grafts were prepared for immunocytochemical staining for LH and FSH. Anterior pituitary glands removed from neonatal (day 1) and day 9 female pups also were stained for LH and FSH. The mean percentage of adenohypophysial cells staining for LH increased from 11% in neonatal pups to mean percentages (24-28%) that were similar in day 9 pups and in all groups with grafts. The mean percentage of adenohypophysial cells staining for FSH increased from 1% in neonatal pups to percentages (16-21%) that were similar in day 9 pups and in grafts in hosts administered 6 or 72 ng LHRH pulses. By contrast, the mean percentage of FSH cells did not increase in grafts in hosts administered vehicle or LHRH by continuous infusion. Serum LH concentration was low in hosts given vehicle or LHRH by continuous infusion but elevated in hosts given 72 ng LHRH pulses and in all but one host given 6 ng LHRH pulses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗