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At least 631 records · Page 35Linked to original sources
PubMed1980

Alteration in the normal pattern of serum testosterone and 5 alpha-androstane-3 alpha, 17 beta-diol in the immature male rat following chronic treatment with luteinizing hormone releasing hormone or luteinizing hormone.

A major component of sexual maturation in the male rat is a progressive decline in serum concentrations of 5 alpha-androstane-3 alpha, 17 beta-diol (3 alpha-diol) and a concomitant increase in testicular testosterone biosynthesis and secretion. Chronic administration of synthetic luteinizing hormone releasing hormone (LHRH) or luteinizing hormone (LH)/human chorionic gonadotropin (hCG) to immature male rats has been shown to result in a delay in sexual maturation as evidenced by decreased sex accessory gland weights and altered testicular testosterone production. We have examined the postulate that such treatments may either reverse or retard the normal developmental pattern of serum testosterone and 3 alpha-diol concentrations. Chronic in vivo treatment of 28 day old immature male rats for 2 weeks with daily injections of either 0.5 micrograms of LHRH, 1.0 micrograms of LHRH, or 30 micrograms of LH was found to result in significant reductions in weights of the seminal vesicles and ventral prostate glands and diminutions in serum testosterone concentrations. Serum content of 3 alpha-diol was either unchanged or slightly elevated in the LHRH treated animals and increased significantly in the LH treated animals. These data suggest that either a reversal of or retardation in the normal developmental pattern of serum testosterone and 3 alpha-diol content has been achieved in the immature male rat by chronic LHRH or LH treatment.

Androstane-3,17-diol↗
PubMed1988

An improved immunogen for anti-human chorionic gonadotropin vaccine eliciting antibodies reactive with a conformation native to the hormone without cross-reaction with human follicle stimulating hormone and human thyroid stimulating hormone.

Beta-subunit of human chorionic gonadotropin (hCG) was associated with alpha-subunit of ovine luteinizing hormone (OLH) to create a heterospecies dimer (HSD) which has a higher steroidogenic potency than the homologous dimer of alpha hCG and beta hCG in the mouse Leydig cell bioassay. The properties and merits of the antibodies induced by this HSD and beta hCG linked to carrier(s) were investigated in rodents and in a subhuman primate species. The antisera had, in both cases, high affinity for binding with hCG (K alpha = 10(9)-10(10) M-1). The mean (+/- S.E.M.) bioneutralization capacity as a percentage of immunoreactivity (determined by radioimmunoassay (RIA)) of the antibodies generated by the HSD-carrier in rats and bonnet monkeys was higher in comparison with those induced by beta hCG linked to carrier (80 +/- 2.3% vs. 63 +/- 1.5% in rats, and 65 +/- 1.9% for HSD vs. 44 +/- 3.7% in monkeys). None of the sera gave any evidence of cross-reactivity with human follicle stimulating hormone (hFSH) and human thyroid stimulating hormone (hTSH).

Animals↗
PubMed1980

Psychological and thyroid-stimulating hormone changes after thyrotropin-releasing hormone in normal women: antagonism by pretreatment with thyroid hormones.

In a double-blind crossover design we treated 20 normal women with thyrotropin-releasing hormone (TRH), 0.5 mg i.v., and saline in a random sequence. Both injections were preceded, 48 hours before, by a single dose of oral thyroid hormones (TH). TRH caused a shift toward mild euphoria, both on objective and subjective ratings. Although statistically significant, the effect was less than that observed in a previous study of normal women in which TH pretreatment was not used. Thus, TH pretreatment appeared partly to block psychological response to TRH. As expected, TH pretreatment also partly blocked thyroid-stimulating hormone (TSH) responses to TRH. Nevertheless, just as in our previous study, psychological responses were significantly negatively correlated with TSH responses. TH appears to exert two independent negative feedback effects: one on the brain (dimished psychological response); and one on the anterior pituitary (diminished TSH response).

Adult↗
PubMed1989

Abnormal thyroid stimulating hormone, prolactin, and growth hormone responses to thyrotropin releasing hormone in abstinent alcoholic men with cerebral atrophy.

The thyroid stimulating hormone (TSH), prolactin (PRL), and growth hormone (GH) responses to thyrotropin releasing hormone (TRH), the Wechsler Adult Intelligence Scale (WAIS) for cognitive impairment, and computed tomographic scans were evaluated in 15 nondepressed alcoholic men after 4 weeks of abstinence and in 10 normal controls. Both cognitive impairment and cerebral atrophy were found in 13 of the alcoholics. Eight alcoholics (seven with cerebral atrophy) had blunted TSH and PRL responses to TRH and a TRH-induced paradoxical increase of GH. This study demonstrates that besides affecting the TSH response to TRH, alcoholism often induces alterations of the PRL and GH secretory patterns in response to TRH. The severe brain damage caused by long-term alcoholism might be involved in the pathogenesis of these neuroendocrine alterations.

Adult↗
PubMed1978

Dissociation of the porcine anterior pituitary: the kinetics of luteinizing hormone release in response to luteinizing hormone-releasing hormone.

A method has been developed for disaggregating porcine anterior pituitary tissue and for providing dissociated preparations which have good, stable viability in culture. The secretory capacity for these preparations in terms of their ability to release luteinizing hormone in response to luteinizing hormone-releasing hormone has been documented in detail. In following the short-term kinetics of LH secretion a biphasic pattern of release has been demonstrated in which a sharp initial peak, maximal at 2 min, is followed by a second, more prolonged phase of release reaching a maximum between 10 and 20 min.

Animals↗
PubMed1979

Interaction of luteinizing hormone-releasing hormone, cyproterone acetate and arginine vasotocin on plasma levels of luteinizing hormone in intact and castrated adult male rats.

Treatment of unanesthetized castrated adult male rats every 3 h for 48 h with either 5 microgram of arginine vasotocin (AVT) and/or 1 microgram luteinizing hormone-releasing hormone (LRH) caused a significant inhibition of plasma levels of luteinizing hormone (LH) and compared to castrated control rats receiving diluent only. However, the intravenous (iv) injection of 1 microgram of AVT into urethane-anesthetized male rats which had been castrated for 0, 24 or 48 h did not affect plasma levels of LH at 10, 20 or 60 min following injection compared to their respective diluent-treated castrated control rats. Similarly, the iv injection of either 100 ng, 1 microgram or 10 microgram AVT was unable to acutely affect plasma levels of LH in intact male rats. Following the iv injection of 2 doses of 50 ng LRH spaced 1 h apart in anesthetized castrated male rats, 2 peaks of equal magnitude in plasma LH were noted. Castrated rats treated with 2 injections spaced 1 h apart of LRH + AVT had significantly higher plasma levels of LH than did rats treated with LRH alone. In subsequent studies, both AVT and arginine vasopressin were observed to augment the plasma response of LH to an injection of LRH whereas oxytocin had no effect. A single injection of AVT + LRH significantly augmented the plasma titers of LH compared to levels observed in LRH-treated control rats as did a second injection 1 h later. The administration of cyproterone acetate sc for 2 days by itself had no effect on plasma LH but in conjunction with LRH caused a marked rise in plasma LH compared to intact rats treated with LRH alone. AVT in combination with LRH and cyproterone acetate caused a significant elevation in plasma LH at 60 min post-injection when compared to plasma levels of rats treated with LRH alone or the combination of LRH and cyproterone acetate. It is concluded that acute intravenous injections of AVT augment the LH-releasing activity of LRH; chronic treatment for 48 h, however, with LRH + AVT leads to a significant depression of plasma LH perhaps due to an exhaustion of the releasable pool of LH in the anterior pituitary.

Animals↗
PubMed1986

Nicotine-induced increases in brain luteinizing hormone releasing hormone-like immunoreactivity and in serum luteinizing hormone levels of the male rat.

By means of radioimmunoassay procedures luteinizing hormone releasing hormone (LHRH)-, Metenkephalin- and somatostatin-like immunoreactivities have been measured in discrete hypothalamic and preoptic nuclei as well as serum luteinizing hormone (LH) levels. Nicotine (2 mg/kg, i.p.) produced after 5 min a significant and selective increase in LHRH-like immunoreactivity in the median eminence and in the medial preoptic nucleus, associated with increases in serum LH levels but without any changes in Met-enkephalin and somatostatin-like immunoreactivities in the median eminence. The results indicate that the nicotine-induced activation of LHRH-immunoreactive neurons involves an enhanced processing of the precursor peptide to LHRH.

Animals↗
PubMed1992

Associated luteinizing hormone-releasing hormone and luteinizing hormone secretion in ovariectomized gilts.

The secretion of luteinizing hormone-releasing hormone (LHRH) and its temporal association with pulses of luteinizing hormone (LH) was examined in ovariectomized prepuberal gilts. Push-pull cannulae (PPC) were implanted within the anterior pituitary gland and LHRH was quantified from 10 min (200 microliters) perfusate samples. Serum LH concentrations were determined from jugular vein blood obtained at the midpoint of perfusate collection. Initial studies without collection of blood samples, indicated that LHRH secretion in the ovariectomized gilt was pulsatile with pulses comprised of one to three samples. However, most pulses were probably of rapid onset and short duration, since they comprised only one sample. Greater LHRH pulse amplitudes were associated with PPC locations within medial regions of the anterior pituitary close to the median eminence. In studies which involved blood collection, LH secretion was not affected by push-pull perfusion of the anterior pituitary gland in most gilts, however, adaptation of pigs to the sampling procedures was essential for prolonged sampling. There was a close temporal relationship between perfusate LHRH pulses and serum LH pulses with LHRH pulses occurring coincident or one sample preceding serum LH pulses. There were occasional LHRH pulses without LH pulses and LH pulses without detectable LHRH pulses. These results provide direct evidence that pulsatile LHRH secretion is associated with pulsatile LH secretion in ovariectomized gilts. In addition, PPC perfusion of the anterior pituitary is a viable procedure for assessing hypothalamic hypophyseal neurohormone relationships.

Animals↗
PubMed2006

A brief review of the addition of gonadotropin-releasing hormone agonists (GnRH-Ag) to growth hormone (GH) treatment of children with idiopathic growth hormone deficiency: Previously published studies from America.

Despite aggressive, early and continuous growth hormone (GH) treatment of children with idiopathic (I) growth hormone deficiency (GHD), height outcomes are often below -1 SDS and do not achieve mid-parental height targets. As pubertal growth accounts for 15% of total growth and gonadotropin-releasing hormone agonist (GnRH-Ag) therapy has successfully prolonged the "prepubertal" growth phase in central precocious puberty, the addition of GnRH-Ag to GH in IGHD has been widely utilized to try to enhance linear growth. Results in the two large GH registry databases and GH prediction models do not support the success of such treatment, although several smaller, controlled trials do indicate some value. Whether GnRH-Ag therapy could be more successful if its use were related to the tempo or age of onset of puberty in a specific child is not known. No universally agreed guidelines exist for the use of GnRH-Ag plus GH in children with GHD or other short stature syndromes and may still be considered experimental.

Age Determination by Skeleton↗
PubMed1978

Inhibitory effect of a luteinizing hormone (LH)-releasing hormone agonist on rat ovarian LH and follicle-stimulating hormone receptor levels during pregnancy.

When injected at the daily dose of 100 microgram on days 7 through 12 of pregnancy, the luteinizing hormone (LH)-releasing hormone (LHRH) agonist [D-Ala6, des-Gly-NH2(10)] LHRH ethylamide led to complete suppression of pregnancy and a 45% to 60% decrease in plasma progesterone concentration. The antifertility effect of the LHRH analog was accompanied by an early and almost complete inhibition of ovarian LH/human chorionic gonadotropin and follicle-stimulating hormone receptor levels. These data suggest that the antifertility effects of LHRH agonists are mediated by down-regulation of ovarian gonadotropin receptors and decreased luteal function.

Animals↗
PubMed1999

Cloning and expression of cynomolgus monkey (Macaca fascicularis) gonadotropins luteinizing hormone and follicle-stimulating hormone and identification of two polymorphic sites in the luteinizing hormone beta subunit.

The genes encoding the cynomolgus monkey gonadotropin subunits, alpha, follicle-stimulating hormone (FSH) beta and luteinizing hormone (LH) beta, were cloned by reverse transcriptase polymerase chain reaction (RT-PCR) using pituitary RNA. The predicted amino acid sequences displayed 82, 96 and 87% identity to human subunit sequences, respectively. Northern blot hybridization of monkey tissues revealed pituitary specific transcripts of 1.0 and 0.6 kb for the alpha and LHbeta subunit, respectively, and two bands of 1.8 and 0.65 kb for the FSHbeta. Upon sequencing LHbeta cDNAs from different monkeys, two polymorphic sites were detected, resulting in the amino acid transitions Ser32Thr and His60Arg. Restriction analysis revealed different homo- and heterozygous combinations of the polymorphic sites indicating linkage dysequilibrium. Transient co-expression of the alpha subunit together with the FSHbeta or LHbeta subunit in COS7 and CHO cells resulted in secretion of in vitro bioactive hormones. This work represents a further step towards production of recombinant monkey LH and FSH which can be used in a homologous experimental setting in the cynomolgus monkey.

Amino Acid Sequence↗
PubMed1999

Growth hormone-releasing hormone receptor (GHRH-R) and growth hormone secretagogue receptor (GHS-R) mRNA levels during postnatal development in male and female rats.

Experimental evidence suggests that differential pituitary sensitivity to hypothalamic signals exerts a role in mediating both age and sex dependent patterns of growth hormone (GH) release and synthesis. One mechanism by which pituitary sensitivity to hypothalamic GH regulators could be modified is by the differential synthesis of their pituitary receptors. In the present report we therefore studied the age and sex dependency of the expression of receptors for two known stimulators of GH release, growth hormone-releasing hormone (GHRH) and the synthetic peptidyl and non-peptidyl GH secretagogues (GHSs). Pituitary GHRH receptor (GHRH-R) and GHS receptor (GHS-R) mRNA levels were measured by reverse transcriptase-polymerase chain reaction (RT-PCR) in male and female rats at postnatal day 1, 10, 30 and 75. We also examined the age- and sex-dependent expression of the GHS-R in whole hypothalamic extracts, since the GHS-R is also expressed in a variety of nuclei within the hypothalamus and has been linked to central regulation of the GH-axis. Pituitary GHRH-R mRNA concentrations were age-dependent; the highest levels were observed in d1 pituitaries and then declined with age, reaching a nadir by d30. These results are in concordance with the age-related decline in pituitary GHRH sensitivity. In contrast, the ontogenic pattern of GHS-R expression was bimodal; GHS-R mRNA concentrations in dl and d30 pituitaries were approximately twice those at d10 and d75. These results mirror the transient increase in GHS sensitivity observed around the onset of puberty, suggesting that gonadal steroids mediate GHS-R expression. GHRH-R mRNA levels were comparable in males and females within each age while GHS-R mRNA levels were gender dependent. At d30, male GHS-R mRNA levels were 30% greater than in their female counterparts. This was reversed at d75, when females had 89% more GHS-R mRNA per pituitary and 65% more per somatotrope than did age-matched males. These sexual differences further support a role for gonadal steroids in the modulation of pituitary GHS-R synthesis. The ontogenic and gender-specific pattern of hypothalamic GHS-R expression differed from that observed for the pituitary. Hypothalamic GHS-R mRNA levels increased with age but exhibited no significant sex difference at each age tested. Taken together, these data demonstrate that changes in the levels of pituitary GHS-R mRNA, but not GHRH-R mRNA, are associated with changes in the gonadal steroid environment, thereby implicating the GHS/GHS-R signalling system as a control point in the establishment and maintenance of sexually dimorphic patterns of GH secretion.

Animals↗
PubMed1986

Effect of luteinising hormone releasing hormone and its analogues on plasma luteinising hormone concentrations in incubating bantam hens.

The ability of synthetic vertebrate luteinising hormone releasing hormones (LHRHs) and their long-acting analogues to maintain elevated plasma luteinising hormone (LH) concentrations and to stimulate ovarian growth was investigated in incubating bantam hens. Chicken LHRH-II (pGlu1-His2-Trp3-Ser4-His5-Gly6-Trp7-Tyr8-Pro9-G ly10-NH2) was more effective than chicken LHRH-I (pGlu1-His2-Trp3-Ser4-Tyr5-Gly6-Leu7-Gln8-Pro9-Gly10-N H2) or porcine LHRH (pGlu1-His2-Trp3-Ser4-Tyr5-Gly6-Leu7-Arg8-Pro9-Gly10-N H2) in stimulating the release of LH. Long-acting analogues of chicken LHRHs (chLHRHs) were created by substituting D-amino acids in position 6. An intravenous injection (10 micrograms/bird) of D-Arg6-chLHRH-II or of a long-acting mammalian analogue of LHRH (buserelin) resulted in a sustained release of LH for up to 8 h. Less sustained releases of LH were observed after the same doses of D-Ala6-chLHRH-I or of D-Trp6-chLHRH-I. Repeated subcutaneous injections of D-Arg6-chLHRH-II or buserelin at 7 to 9 h intervals for 9 d resulted in loss of pituitary gland responsiveness to these analogues. For this reason, the treatment failed to maintain elevated plasma LH concentrations and did not stimulate the growth of the ovary or oviduct.

Animals↗
PubMed1992

Comparison of the basal and luteinising hormone-releasing hormone induced luteinising hormone release by perifused hypophyses from turkey hens (Meleagris gallopavo) at different physiological stages.

1. An experiment was performed to investigate the weight of the ovary, the oviduct, the pituitary gland, the plasma concentrations of luteinising hormone (LH), progesterone, oestradiol and the responsiveness of the pituitary gland in vitro to doses of Luteinising Hormone-Releasing Hormone (LH-RH) ranging from 10(-10) to 10(-5) M in laying (L), incubating (I) and out-of-lay (OL) turkey hens. 2. Pituitary weights did not differ between the groups but the weights of the ovary and oviduct and the plasma concentrations of progesterone and oestradiol were lower in I and OL than in L hens. The plasma concentrations of LH were lower in I than in L hens. 3. In vitro, the basal release of LH was similar in L and I hens, but significantly higher in OL hens. A slow and linear increase in basal LH release by the glands from I and OL hens was observed throughout the experiment. 4. No clear dose-response relationship was found in any of the reproductive states with respect to LH release in vitro following LH-RH stimulation, probably as a result of partial cell desensitisation. On the other hand, the amount of LH released over basal level in responses to stimulation with different doses of LH-RH were not significantly different between L and I hens, but they were between 5- to 10-fold higher in OL hens, except at the lowest dose. 5. These findings confirm that there is no correlation between circulating LH in turkey hens and the capacity of the hypophysis to release LH in vitro passively or in response to LH-RH. Therefore, the low circulating concentrations of LH in I and OL turkey hens cannot be accounted for by decreased adenohypophyseal responsiveness to LH-RH. They may indicate a low level of hypothalamic secretion of LH-RH and/or to the existence of an inhibitory mechanism on LH secretion in vivo in both OL and I hens.

Analysis of Variance↗
PubMed1993

Precocious puberty in tamoxifen-treated cockerels: hypothalamic gonadotrophin-releasing hormone-I and plasma luteinising hormone, prolactin, growth hormone and testosterone.

1. The administration of the anti-oestrogen, tamoxifen (TAM) to juvenile chicks results in precocious puberty. In the present study the effects of TAM administration (1 mg/kg body weight on alternate days from 12 d of age) on testicular function, hypothalamic chicken gonadotropin-releasing hormone (cGn-RH-I), plasma luteinising hormone (LH), growth hormone (GH), prolactin (PRL) and testosterone were studied in juvenile White Leghorn cockerels. 2. The increase in hypothalamic GnRH-I content which occurs during sexual development was advanced in TAM-treated birds, in association with precocious testicular development, an early rise of plasma testosterone content and enhanced comb growth. 3. Plasma LH concentrations behaved similarly and were higher in the TAM-treated than in control birds, during most of the experimental period. Plasma PRL concentration, which is high at hatching, decreased more quickly in TAM-treated than in control birds; plasma GH values were not consistently affected by TAM treatment. 4. Both the growth and the involution of the bursa of Fabricius in the TAM-treated cockerels preceded that in the control chicks. 5. It is concluded that TAM treatment induces precocious puberty in the cockerel by blocking the negative feedback action of aromatised testicular androgens on the hypothalamus.

Animals↗
PubMed1993

Induced moulting in cockerels: effects on sperm production, plasma concentrations of luteinising hormone, testosterone and thyroxine, and on pituitary sensitivity to luteinising hormone-releasing hormone.

1. The ability of a moult-inducing procedure to restore high levels of sperm production was assessed, in two experiments, using cockerels with reduced sperm production. The moulting procedure consisted of a period of food and light restriction for 6 weeks. The moulted birds were compared with control birds for 20 weeks. 2. Moult induction resulted in decreased daily sperm output (DSO) and plasma testosterone concentration, from weeks 3 to 7. In the first experiment, plasma luteinising hormone (LH) concentration in moulted birds was reduced on week 5. 3. No change in pituitary sensitivity to chicken luteinising hormone-releasing hormone-I (cLHRH-I) was detected at week 3 in moulted cockerels. In moulted birds, a transient increase in plasma thyroxine concentration was detected. 4. After the end of moult induction, testosterone concentrations increased, plasma LH showed a rebound at week 7 and the pituitary sensitivity to LHRH was increased at week 9. 5. This increased activity of the pituitary-testicular axis resulted for a short time in an increase in DSO of moulted birds compared with that of controls. Although amelioration was moderate, this result indicates the possibility of improving sperm production in the cockerel by using an induced moulting procedure.

Animals↗
PubMed1982

Temporal patterns of serum luteinizing hormone and testosterone and endocrine response to luteinizing hormone releasing hormone in aging male rats.

Temporal patterns of serum testosterone and luteinizing hormone (LH) concentration and responsiveness to luteinizing hormone releasing hormone (LHRH) were measured in young (2 to 3 months), middle-aged (12 to 13 months), and aged (22 to 26 months) male rats. Average testosterone and LH concentrations, as well as individual sample variations, were higher in young than in middle-aged and aged rats and higher in middle-aged than in aged groups. In addition, the young group showed a diurnal pattern of serum testosterone concentration and greater ranges of LH and testosterone concentrations in individual blood samples. Young male rats showed greater increases in serum LH and testosterone than middle-aged and aged groups after intravenous LHRH, 1 and 5 ng/g of body weight. These data indicate that LH and testosterone secretion are progressively reduced in the aged male rat and suggest alterations in neuroendocrine control of pituitary gonadotropin secretion as the most important alteration in the gonadal control system in these animals.

Aging↗
PubMed1984

Direct inhibitory effect of estradiol on pituitary luteinizing hormone responsiveness to luteinizing hormone releasing hormone is specific and of rapid onset.

We have employed a perifusion technique to explore the time course and specificity of 17 beta-estradiol (E2) effects directly upon luteinizing hormone (LH) release from the isolated rat anterior pituitary under pulsatile luteinizing hormone releasing hormone (LHRH) stimulation. We first characterized the perifusion system and fitted the data to a simple dose-response model. Multiple perifusion studies were then performed with pulses of LHRH at approximately half-maximal response concentration (10(-8) M); LH responses to an initial LHRH pulse (#1) were compared with LH responses to a second LHRH pulse (#2) given at variable times after addition of E2, antiestrogen (LY 117018), and/or 17 alpha-estradiol (17 alpha-E2). Using this approach, we found that the direct inhibitory effect of E2 upon LH responsiveness to LHRH was rapid and specific. The ratio of LH secretion in response to LHRH pulse #2 to that in response to LHRH pulse #1 (LH secretion ratio) decreased steadily during 1 h of exposure to E2. This inhibition was significant (P less than 0.01) by 36 min of E2 exposure. It represented more than the removal of a LHRH self-priming effect because the LH secretion ratios were significantly less than 1.0 [0.80 +/- 0.05 (SEM), P less than 0.01] within 36 min of E2 exposure. The inhibitory effect was not seen when LY 117018 was added with E2, nor when 17 alpha-E2 replaced E2. The specificity of this rapid E2 inhibitory effect upon pituitary LH responsiveness to LHRH strongly suggests that it is receptor mediated. The rapidity of this apparent receptor-mediated estrogen effect suggests that it is a very rapid consequence of nuclear translocation of the E2-receptor complex.

Animals↗