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PubMed2003

Dynamics of subcellular organelles, growth hormone, Rab3B, SNAP-25, and syntaxin in rat pituitary cells caused by growth hormone releasing hormone and somatostatin.

Rab3B is involved in the exocytosis of synaptic vesicles and secretory granules in the central nervous system and the anterior pituitary cells. The aim of this study was to elucidate both the role of rab3B in GH secretion and the mutual relationship of rab3B and SNARE proteins. Adult male rats were injected intravenously with 10 microg of growth hormone releasing hormone (GHRH) or 10 microg of somatostatin (SRIF). Untreated rats were used as controls, and their pituitary glands were sectioned for histochemical examination. Rab3B is localized on the limiting membrane of the secretory granules and the cytosol. Confocal laser scanning microscopic observation of immunohistochemical double staining of rab3B and GH revealed that immunoreactivity of rab3B increased in GHRH-treated rats and decreased in SRIF-treated rats. Confocal laser scanning microscopic observation of immunohistochemical double staining of SNAP-25, syntaxin, and rab3B revealed the co-localization of rab3B and these SNARE proteins in GHRH-treated rats, and their dissociation in SRIF-treated rats. These results suggest that rab3B plays a principal role in GH secretion in the anterior pituitary cells and that SNAP-25 and syntaxin act as co-workers with rab3B in the functional regulation of GH secretion.

Animals↗
PubMed1987

An immunohistochemical study of adenohypophyseal cells containing follicle-stimulating hormone and luteinizing hormone during the phase of selective follicle-stimulating hormone release in postnatal female rats.

Serum concentration of follicle-stimulating hormone (FSH) in the juvenile female rat increases independently from that of luteinizing hormone (LH). The objective of this study was to determine whether this increase in serum FSH is accompanied by a proliferation of FSH-cells greater than the proliferation of LH-cells. Thus, we measured circulating FSH and LH in female rats on days 3, 10, 13, 17, and 20, calculated the percentages of adenohypophyseal cells that contained FSH or LH on days 3, 10, and 20, and determined whether cells containing only FSH existed on day 10. Serum FSH concentrations on days 10 and 13 were significantly greater than those on days 3, 17, or 20. No differences existed in serum LH concentrations. Cells containing FSH or LH were distributed throughout the entire adenohypophyses of 3, 10, and 20-day-old females. Clusters of these cells were observed in the ventral regions of adenohypophyses of 3-day-old females. The percentages of adenohypophyseal cells containing FSH increased significantly from approximately 9% in 3-day-old rats to approximately 17% in 10-day-old rats and then decreased to approximately 14% in 20-day-old animals. At all ages the percentages of adenohypophyseal cells containing FSH were similar to the percentages of cells containing LH. At 10 days of age, all cells containing FSH also contained LH and all cells containing LH also contained FSH. These data suggest that the increase in serum FSH in the juvenile female rat is associated with an increase in the percentage of adenohypophyseal cells containing FSH and that at this time all cells containing FSH also contain LH.

Aging↗
PubMed1979

Subcellular distribution of brain peptidases degrading luteinizing hormone releasing hormone (LHRH) and thyrotropin releasing hormone (TRH).

The luteinizing hormone and thyrotropin-releasing hormones have been shown to be mostly concentrated in the nerve endings of the median eminence. In contrast, the peptidases responsible for their degradation present an ubiquitous localization and most of the reports have dealt with the total soluble activity. A detailed study of the subcellular distribution of these enzymes was thus performed in cerebral cortical and hypothalamic preparations of rat brain. The activity of a soluble marker, lactic dehydrogenase, was also measured to control for possible contaminants. The results showed that only 10% of peptidase activity was present in the nerve ending preparation. Evidence is provided for a non-neglible membrane-bound enzymatic component responsible for TRH degradation at the synaptosomal level of both cortex and hypothalamus.

Animals↗
PubMed1990

In vivo and in vitro studies on the effect of the serotoninergic system on luteinizing hormone and luteinizing hormone-releasing hormone secretion in prepubertal and peripubertal female rats.

The present investigations were designed to assess the effect of the serotoninergic system on luteinizing hormone (LH) and LH-releasing hormone (LH-RH) secretion in female rats aged 14 and 30 days. The administration of 5-hydroxytryptophan (5-HTP; 75 mg/kg i.p.) increased hypothalamic serotonin (5-HT) concentrations in both age groups, and did not affect hypothalamic norepinephrine (NE) concentrations or release. Serum LH levels were raised by 5-HTP in 14-day-old, but not in 30-day-old rats. Basal and KCl- (28 mM) stimulated LH-RH release by incubated hypothalamic fragments was significantly enhanced when 5-HTP was injected previously to 14-day-old animals. In 30-day-old rats, 5-HTP treatment did not modify basal LH-RH release, and decreased the KCl-stimulated LH-RH output. Similarly, the addition of 5-HT (10(-7) M) to superfused hypothalamic fragments enhanced basal LH-RH release in 14-day-old rats and blocked the increment in LH-RH release evoked by KCl in 30-day-old rats. The present results show that in 14-day-old female rats, the serotoninergic system (activated in vivo by 5-HTP treatment, or in vitro by 5-HT addition) exerts a stimulatory effect on LH-RH, and thus, on LH release. On the contrary, in 30-day-old animals, stimulated LH-RH secretion was inhibited by 5-HT. Apparently, the hypothalamic NE system is not implicated in this response. The participation of this changing effect of 5-HT on LH-RH/LH release at the onset of puberty is postulated.

5-Hydroxytryptophan↗
PubMed1991

Human growth hormone-releasing hormone analogues with much improved in vitro growth hormone-releasing potencies in rat pituitary cells.

Enhancement of the amphiphilic alpha-helical properties of the central and C-terminal regions of growth hormone-releasing hormone (GRH) by substitution with helix-favouring amino acids, particularly Ala, can result in significant improvements in GH-releasing potencies using monolayer cultures of rat pituitary cells, a system which reflects analogue receptor affinity rather than effects of structural modifications on pharmacokinetic properties. For instance, previously reported, helix-enhanced [Ala15]GRH-(1-29)NH2 was presently 5 times more potent than [Gly15]GRH-(1-29)NH2 in this assay. The extent and importance of alpha-helical character further towards the N-terminus is less clear since Chou-Fasman probability calculations indicate also the possibility of beta-bend formation in the 6-10 region. However, replacement of Asn8 with Ala resulted in a 4-fold improvement in potency and when this was combined with Ala15 to give [Ala8,15]GRH-(1-29)NH2 a 15-fold increase in potency was achieved and combination of D-Ala2, Ala8 and Ala15 gave a 27-fold increase indicating that the effects of all of these modifications were additive. Computer analysis furthermore revealed that substitution of Ala for Ser in position 9 should also increase alpha-helix probability from 0.93 to 1.05. [D-Ala2,Ala8,9,15]GRH- (1-29)NH2 was 49 times more potent than GRH itself making it by far the most potent analogue thus far reported in an in vitro assay system. The Ala8 and Ala9 substitutions were also effective in improving the inhibitory potency of a GRH receptor antagonist, [D-Arg2,Leu27]GRH-(1-29)NH2.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1988

Induction of ovulation and oviposition in female quail with luteinizing hormone, luteinizing hormone releasing hormone, or progesterone.

Regularly laying female Japanese quail were injected 12 or 18 hr before the next expected oviposition with 25 micrograms oLH, 25 micrograms luteinizing hormone releasing hormone (LHRH), or 0.05 mg progesterone, and the subsequent oviposition was recorded and ovulation determined by autopsy 9 hr after the injection. Plasma progesterone levels were measured in blood collected from a wing vein during the postinjection interval. Vehicle-injected birds served as control. All treatments resulted in premature oviposition and ovulations in 50-100% of birds when injected 12 hr before the next expected oviposition. None of the vehicle-injected birds showed any advancement in either oviposition or ovulation. Premature oviposition was generally followed by premature ovulation within 1 hr, when birds were treated 12 hr before the next expected oviposition and was preceded by a rise in plasma progesterone levels which reached values similar to those occurring during the normal preovulatory period. When birds were injected 18 hr before the next expected oviposition, the incidence of premature oviposition was very low, premature ovulation was absent, and the rise in plasma progesterone levels following treatment was substantially less than in the former group. The results suggest that oviposition and ovulation in quail may be initiated by LHRH induced LH release from the pituitary gland and that progesterone may stimulate LHRH and LH release. The timing of the ovulatory cycle may depend upon the phase of follicular maturation.

Animals↗
PubMed1985

Luteinizing hormone releasing hormone mediates naloxone's effects on serum luteinizing hormone levels in normal and morphine-sensitized male rats.

Naloxone produces large increases in serum luteinizing hormone (LH) levels in normal males and females, supporting a role for endogenous opioids (EOP) in the tonic inhibition of LH. Since the antagonist apparently exerts no important effects on the pituitary, the reasonable assumption has been made that it elevates gonadotropin levels by affecting the release of LH-releasing hormone (LHRH) from the hypothalamus. However, at present there is no direct in vivo evidence supporting this widely-held view. In an attempt to directly demonstrate that naloxone increases the secretion of LHRH, and thereby elevates serum LH levels, we examined whether a potent synthetic antagonist of LHRH ( [D-p Glu1, D-Phe2, D-Trp3,6]-LHRH, GPT-LHRH) blocked the effects of naloxone in male rats with a normal response to naloxone and in those with a markedly enhanced sensitivity to the drug induced by a brief period of morphine pellet implantation. Our results demonstrated that GT-LHRH antagonized equipotent doses of LHRH (100 ng/kg) and naloxone (0.5 mg/kg) over a similar time course with approximately the same AD50. Most importantly, however, we showed that the GPT-LHRH produced equivalent, parallel shifts to the right in the dose-response curves for LHRH and naloxone, indicative of competitive inhibition. We also found that GPT-LHRH completely abolished the enhanced response to naloxone's effects on LH which occurs in morphine-pretreated rats. Since we observed no competition between LHRH and naloxone for their binding sites in pituitary or brain, the only viable interpretation of our results is that naloxone increases LH by inducing the release of LHRH.

Animals↗
PubMed1990

Triiodothyronine administration reduces serum growth hormone levels and growth hormone responses to thyrotropin-releasing hormone in patients with anorexia nervosa.

The aim of this study was to test the hypothesis that low serum T3 concentrations may promote an abnormal growth hormone (GH) response to thyrotropin-releasing hormone (TRH) in patients with anorexia nervosa. Eight anorexic women and two anorexic men, ages 15-25 years, with low free T3 circulating levels (mean +/- SEM = 2.8 +/- 0.3 pmol/l) were studied. A TRH test (200 micrograms IV) was carried out under basal conditions and repeated following treatment with oral T3 (1.5 micrograms/kg BW/day) for eight days. Following T3 administration, GH levels dropped significantly from a baseline of 7.1 +/- 1.3 micrograms/l to 3.1 +/- 0.7 micrograms/l (p less than 0.02), as did GH peak responses to TRH (9.0 +/- 1.0 micrograms/l vs 4.4 +/- 0.8 micrograms/l, p less than 0.01). ANOVA and analysis of area under the curve (AUC) confirmed that after T3 treatment there was a significant reduction in TRH-induced GH release in these patients (GH AUC: 902 +/- 132 micrograms/l vs. 456 +/- 91 micrograms/l, p less than 0.02). TSH responses to TRH, which were normal prior to T3 treatment, completely disappeared following it, and PRL responses to TRH also were diminished. Although our experimental approach does not permit a conclusion that low T3 levels were the primary reason for these changes, the data support the theory that low T3 circulating levels may facilitate abnormal GH secretion and the GH-releasing activity of intravenous TRH.

Adolescent↗
PubMed1991

Luteinizing hormone in the bovine pars tuberalis: secretion in response to luteinizing hormone releasing hormone and intracellular isoforms.

The objective of this study was to examine the physiological characteristics of gonadotropes in the bovine (b) pars tuberalis as assessed by their ability to release Luteinizing Hormone (LH) in response to LH-Releasing Hormone (LHRH) and the intracellular distribution of LH isoforms. At slaughter, the stalk median eminence and associated pars tuberalis as well as the anterior pituitary gland were collected from each of 7 castrate males. Each stalk median eminence and pituitary gland was mid-sagitally sectioned and weighed. One half of each tissue was immediately frozen and subsequently homogenized to determine the intracellular distribution of bLH isoforms. Tissue extracts were desalted by flow dialysis against water and chromatofocused on pH 10.5-7.0 gradients. The remaining half of the pituitary was sliced with a Staddie-Riggs slicer. The pituitary slices and the remaining half of the stalk median eminence were perifused (0.1 ml/min) for a total of 360 min with effluent samples (1.0 ml) collected every 10 min. At 130 min tissues were stimulated with 5 x 10(-8) M LHRH. Concentrations of LH in the effluent samples and the fractions collected from chromatofocusing were determined by radioimmunoassay. The release of LH in response to LHRH was 43.9% and 47.0% above basal secretion for the pars tuberalis and pituitary, respectively, suggesting similar degrees of responsiveness. Pars tuberalis and pituitary extracts resolved into nine LH isoforms during chromatofocusing and were coded with letters beginning with the most basic form. No differences (P greater than .05) were observed in distribution of LH isoforms between the pars tuberalis and the pituitary gland.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Changes in serum luteinizing hormone (LH) concentrations in response to luteinizing hormone releasing hormone (LHRH) in bull calves that attained puberty early or late.

The objectives of this study were to determine if the response to luteinizing hormone releasing hormone (LHRH) could be used to select bull calves capable of early sexual maturation and to establish the optimum route and dose of LHRH. In Trial 1, at 4, 10 and 20 week of age, 20 calves were treated iv with 2 microg/kg body weight of LHRH 1 and 5h after commencing a 9-h period of blood sampling. Bulls were separated into early and late maturing (n=10), based on age at puberty (scrotal circumference (SC) of >or=28 cm). At 4 and 20 week of age, peak serum LH concentrations and area under the LH response curve in response to LHRH were lower (P<0.05) in early- versus late-maturing bulls. In Trial 2, calves at 20 week of age were given LHRH as follows: 2 microg/kg body weight iv (n=6), im (n=6) or sc (n=6); 5 microg/kg im (n=6), or ischio-rectally (ir, n=6) or sc (n=6); and 10 microg/kg im (n=6) or sc (n=6). Serum LH concentrations were at a plateau from 30 to 165 min after treatment with 5 microg/kg of LHRH (im or ir; P>0.05). We concluded that the LH responses to LHRH in calves at 4 and 20 week of age could facilitate the development of a simple test (one blood sample prior to treatment with LHRH and a second during the period of sustained response to LHRH) to select early-maturing bulls.

Age Factors↗
PubMed2002

Luteinizing hormone and luteinizing hormone-releasing hormone secretion is under locus coeruleus control in female rats.

It has been suggested that norepinephrine (NE) from the locus coeruleus (LC) plays an important role in triggering the preovulatory surge of gonadotropins. This work intended to study the role of LC in luteinizing hormone (LH) secretion during the estrous cycle and in ovariectomized rats treated with estradiol and progesterone (OVXE(2)P) and to correlate it with LH releasing hormone (LHRH) content in the medial preoptic area (MPOA) and median eminence (ME). Female rats on each day of the estrous cycle and OVXE(2)P were submitted to jugular cannulation and LC electrolytic lesion or sham-operation, at 09:00 h. Blood samples were collected hourly from 11:00 to 18:00 h, when animals were decapitated and their brains removed to analyze LC lesion and punch out the MPOA and ME. Plasma LH levels and LHRH content of MPOA and ME were determined by radioimmunoassay. During metestrus, diestrus and estrus, LC lesion did not modify either LH plasma concentrations or LHRH content, but completely abolished the preovulatory LH surge during proestrus and the surge of OVXE(2)P. These blockades were accompanied by an increased content of LHRH in the MPOA and ME. The results suggest that: (1). LC does not participate in the control of basal LH secretion but its activation is essential to trigger spontaneous or induced LH surges, and (2). the increased content of LHRH in the MPOA and ME may be due to a decreased NE input to these areas. Thus, LC activation may be required for depolarization of LHRH neurons and consequent LH surges.

Animals↗
PubMed1997

Progesterone blockade of a luteinizing hormone surge blocks luteinizing hormone-releasing hormone Fos activation and activation of its preoptic area afferents.

Progesterone is capable of facilitating or blocking the luteinizing hormone (LH) surge, depending on the timing of its administration. However, the precise targets of progesterone's actions are unknown. Since recent studies described the presence of a periventricular preoptic area (pePOA) neuron population afferent to LH-releasing hormone (LHRH) neurons that is co-activated to express c-Fos with LHRH neurons at the time of the LH surge, the present study was designed to determine if the pePOA neurons contain progesterone receptors (PRs) and whether progesterone inhibition is manifested by a failure of LHRH and pePOA neurons to become activated at the time of an LH surge. For progesterone facilitation, a group of immature rats each received a silastic capsule (1.57 mm i.d., 3.18 mm o.d., 1.5 cm long) containing estradiol-17beta (E2) in peanut oil (150 microg/ml) at 09.00 h on postnatal day 28 followed 24 h later by a progesterone implant (crystalline, 1.57 mm i.d., 3.18 mm o.d., 1.5 cm long). For progesterone inhibition, a second group of rats received the estrogen capsule and a progesterone capsule (3.35 mm i.d., 4.65 mm o.d., 3.0 cm long) together at 09.00 h on day 28, and 24 h later received only a blank capsule. On the afternoon of postnatal day 29, all animals were anesthetized and perfused for localization of c-Fos and LHRH, PRs alone, or c-Fos and PRs. The present studies determined that following a progesterone-inhibition paradigm, along with blockade of the LH surge, both activation of LHRH and pePOA neurons was low or absent. Staining of PRs in progesterone-facilitated and progesterone-inhibited rats indicated that the pePOA neurons contained PRs in similar patterns. Double labeling of c-Fos and PRs in progesterone-facilitated rats indicated that nearly all the c-Fos-positive neurons of the pePOA (80 +/- 4.2%) co-expressed PRs; in progesterone-inhibited rats, only 32 +/- 12% of few c-Fos-positive neurons also contained PRs. In no instance were LHRH neurons found to contain PRs. Taken together, these data suggest that both progesterone facilitation and inhibition likely involve direct actions of progesterone on the pePOA neurons, and are consistent with a role for the pePOA neurons in transducing steroid effects on LHRH neurons.

Animals↗
PubMed1976

Correlation between leuteinizing hormone responses to luteinizing hormone-releasing hormone (LH-RH) and to D-leu-6-LH-RH-ethylamide in patients with hypothalamo-pituitary disease.

Seventeen patients (eleven females and six males) with organic hypothalamo-pituitary disease were subjected to a test consisting of a rapid intravenous injection of 50 mug of luteinizing hormone-releasing hormone (LH-RH) at 8:00 A.M., with blood sampling before and 30 and 60 minutes afterward. Two to four weeks later, a rapid intravenous injection of 50 mug of D-Leu-6-des-Gly-10-LH-RH-ethylamide (D-Leu-6-LH-RH-EA) was given under similar conditions, with blood sampling before and 30, 60, and 90 minutes afterward. Serum LH levels were determined by radioimmunoassay. D-Leu-6-LH-RH-EA caused a greater and more sustained rise in serum LH levels than did an equal dose of LH-RH. However, functional classifications of patients were similar with either preparation. This finding suggests that acute administration of D-Leu-6-LH-RH-EA does not cause a higher number of relevant responses as compared with LH-RH, but only a greater stimulation of LH releases in responsive patients.

Adenoma, Acidophil↗
PubMed1987

Thyroid hormone receptor binds to a site in the rat growth hormone promoter required for induction by thyroid hormone.

Transcription of the rat growth hormone (rGH) gene in pituitary cells is increased by addition of thyroid hormone (T3). This induction is dependent on the presence of specific sequences just upstream of the rGH promoter. We have partially purified T3 receptor from rat liver and examined its interaction with these rGH sequences. We show here that T3 receptor binds specifically to a site just upstream of the basal rGH promoter. This binding site includes two copies of a 7-base-pair direct repeat, the centers of which are separated by 10 base pairs. Deletions that specifically remove the T3 receptor binding site drastically reduce response to T3 in transient transfection experiments. These results demonstrate that T3 receptor can recognize specific DNA sequences and suggest that it can act directly as a positive transcriptional regulatory factor.

Animals↗
PubMed1990

Luteinizing hormone-releasing hormone neurons express Fos protein during the proestrous surge of luteinizing hormone.

The ability of luteinizing hormone-releasing hormone (LHRH) neurons to express the oncogene c-fos was examined during the estrous cycle in rats. The immunocytochemical localization of the c-fos-encoded antigen, Fos, was coupled with the immunocytochemical localization of LHRH. LHRH neurons showed no Fos immunoreactivity during diestrus-1, diestrus-2, estrus, or the morning of proestrus. However, Fos was expressed in LHRH neurons from 1600 to 2200 hours during proestrus. The timing of onset of Fos expression in LHRH neurons during proestrus suggests a strong correlation with increased LH secretion. Pentobarbital, which blocks the preovulatory LH surge, blocked Fos expression in LHRH neurons, but the LHRH neurons expressed Fos on the following afternoon at the time of the expected delayed LH surge. Not all LHRH neurons expressed Fos during the LHRH surge. Approximately half of the LHRH neurons were activated in the preoptic area and anterior hypothalamus; more anteriorly positioned LHRH neurons did not express Fos, resulting in an overall stimulation of 40% of the LHRH neurons. These data provide direct evidence that stimulation of LHRH neurons during proestrus takes place at the LHRH cell bodies, and identify the specific population of LHRH neurons which are activated.

Animals↗
PubMed2001

Growth hormone-releasing factor affects macronutrient intake during the anabolic phase of zinc repletion: total hypothalamic growth hormone-releasing factor content and growth hormone-releasing factor immunoneutralization during zinc repletion.

Growth hormone-releasing factor (GRF) is thought to perform two distinct functions within the brain. GRF synthesized in the median eminence (ME) stimulates the release of growth hormone (GH) from the pituitary, while GRF in the suprachiasmatic nucleus and median preoptic area (SCN/MPOA) may stimulate selection of dietary protein. These two functions may be coupled to regulate and enhance growth. During zinc repletion, a period characterized by increased protein intake and accelerated growth, we examined this coupling by measuring GRF peptide content in hypothalamic sites and neutralizing GRF function by infusing anti-GRF antibody into the hypothalamus during zinc repletion. Total GRF content and GRF content in the ME and SCN/MPOA were decreased in zinc-deficient (Zn-) rats compared to zinc-adequate (Zn+) rats (P < 0.05). There were no differences in GRF content during zinc repletion in either nuclei. Subsequently, we investigated the macronutrient feeding patterns of rats chronically infused with anti-GRF IgG into the lateral ventricle of the brain during zinc repletion. All Zn- and Zn+ rats administered anti-GRF IgG exhibited a reduction in protein intake during zinc repletion. The Zn- rats receiving anti-GRF-IgG consumed equal amounts of total diet compared to those receiving vehicle during the repletion period however they consumed less carbohydrate (P < 0.05) and considerably more fat (P < 0.02). There were no significant differences in carbohydrate or fat intake in Zn+ rats receiving anti-GRF antibody. These results suggest that GRF likely directs protein intake during normal growth, but may interact with additional appetite-controlling neuropeptides during zinc repletion.

Animal Nutritional Physiological Phenomena↗
PubMed1999

The value of basal serum follicle stimulating hormone, luteinizing hormone and oestradiol concentrations following pituitary down-regulation in predicting ovarian response to stimulation with highly purified follicle stimulating hormone.

The value of gonadotrophin and oestradiol concentrations following pituitary down-regulation with leuprolide acetate in predicting ovarian response to stimulation was evaluated in three groups of women undergoing ovarian stimulation for in-vitro fertilization with highly purified follicle stimulating hormone (FSH). Leuprolide acetate was started in the midluteal phase, and either stopped at menses (IVF-SL group, n = 3), or continued throughout stimulation (IVF-LL group, n = 38; oocyte donors, n = 58). Ovarian stimulation was started on cycle day 3, after blood was drawn for down-regulated FSH, luteinizing hormone (LH) and oestradiol. Higher down-regulated LH was predictive of higher oestradiol on day 5 of stimulation in both IVF groups, and of need for fewer ampoules in the IVF-LL group, but not of oestradiol on day of human chorionic gonadotrophin (HCG) administration or number of oocytes retrieved. Higher FSH after down-regulation predicted yield of fewer oocytes in the donor and IVF-LL groups, and higher oestradiol on day 5 of stimulation, need for fewer ampoules and a shorter duration of therapy in both IVF groups. Higher oestradiol after down-regulation was associated with higher oestradiol on day 5 of stimulation and on day of HCG administration, a shorter duration of therapy and need for fewer ampoules in all groups. Whereas these results do not ascribe any predictive significance to LH, they suggest that oestradiol and FSH concentrations after down-regulation are predictive of the pattern of ovarian response to stimulation and of oocyte yield.

Adult↗
PubMed2000

Short-term recombinant human growth hormone therapy does not modify growth hormone, thyrotropin and prolactin responses to thyrotropin-releasing hormone in adult dialysis patients.

BACKGROUND: We recently have reported the first randomized, controlled study on the effects of short-term recombinant human growth hormone (rhGH|| therapy on the nutritional status of a group of malnourished adult dialysis patients. In order to evaluate whether rhGH administration exerts any influence on GH, thyrotropin (TSH|| and prolactin (PRL|| responses to TSH-releasing hormone (TRH||, we assessed these responses before and after rhGH therapy. METHODS: GH, PRL and TSH responses to TRH before and 1 month after rhGH therapy in a group of adult dialysis patients were evaluated. Seventeen dialysis patients (11 on continuous ambulatory peritoneal dialysis/six on haemodialysis|| were studied (rhGH group, n=8; control group, n=9||. In the rhGH group, 0.2 IU/kg/day rhGH was administered subcutaneously. Each patient was tested with TRH (400 microg bolus i.v.|| on two separate occasions, just before and immediately after the treatment period. RESULTS: rhGH treatment did not modify baseline serum GH concentrations (6.6+/-2.7 vs 4.1+/-1.1 microg/l||, paradoxical GH responses to TRH (six out of eight patients||, GH peak (11.9+/-4.6 vs 11.2+/-5.3 microg/l, NS|| or area under the secretory curve of GH (GH AUC; 19.1+/-4.5 vs 12.1+/-3.1 microg/h/l||. Both basal PRL (35.5+/-7.1 vs 36.7+/-8.6 microg/l|| and TSH (2.3+/-1.1 vs 2.8+/-1.7 mU/l|| concentrations, as well as their responses to TRH stimulation (PRL peak, 59.9+/-16.6 vs 59. 5+/-11.8 microg/l; TSH peak, 6.2+/-2.6 vs 7.1+/-3.9 mU/l||, were also unaffected by rhGH therapy. CONCLUSION: These results suggest that short-term rhGH therapy does not significantly influence the magnitude of the somatotropic, lactotropic or thyrotropic response to TRH in adult dialysis patients. However, this finding has to be interpreted with caution due to the two different patient groups included in this study.

Adult↗