[Regulation of the adenohypophysis by hypothalamic hormones. Biochemistry and physiology of releasing hormones. IV. Somatostatin and somatotropin releasing hormones].
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Animals↗
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Hormonal regulation of gene expression: regulation of growth hormone gene transcription by growth hormone releasing factor.
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Animals↗
Gonadotropin and prolactin secretion in human pseudocyesis: effect of synthetic luteinizing hormone-releasing hormone (LH-RH) and thyrotropin releasing hormone (TRH)
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Female↗
Studies in the use of luteinizing hormone-follicle-stimulating hormone releasing hormone to induce ovulation in women.
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Adult↗
Chemistry of hypothalamic neurohormones. Synthesis and structure-activity relationship studies of thyrotropin-releasing hormone and luteinizing-hormone-releasing hormone.
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Amino Acid Sequence↗
Isolation of the luteinizing hormone and follicle-stimulating hormone-releasing hormone from porcine hypothalami.
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Amino Acids↗
Effects of cloprostenol and prostaglandin F2 alpha on secretion of follicle stimulating hormone, luteinizing hormone, prolactin, growth hormone, thyroxine and cortisol in heifers.
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Animals↗
[Action of growth hormone releasing hormone (GHRH) on sleep EEG and nocturnal secretion of growth hormone, cortisol and ACTH in patients with major depression].
In contrast to the effects of GHRH in young normal human subjects, in which repetitive i.v. administration of GHRH prompts an increase in the amount of slow wave sleep (SWS) and in GH secretion and blunting of cortisol release, both in young and in old patients with depression there is no effect on SWS and cortisol release after GHRH, while GH secretion is stimulated. We assume that HPA activity and SWS are inert to the influence of GHRH during acute depression because of a slight CRH overactivity, whereas GHRH exerts effects on GH secretion.
Adrenocorticotropic Hormone↗
Thyroid hormone for preventing of neurodevelopmental impairment in preterm infants.
BACKGROUND: Observational studies have shown an association between transiently low thyroid hormone levels in preterm infants in the first weeks of life (transient hypothyroxemia) and an abnormal neurodevelopmental outcome. Thyroid hormone therapy might prevent this morbidity. OBJECTIVES: To assess whether thyroid hormone therapy in preterm infants without congenital hypothyroidism results in clinically important changes in neonatal and long term outcomes in terms of both benefits and harms. SEARCH STRATEGY: The standard search strategy of the Neonatal Review Group was used. This included searches of the Oxford Database of Perinatal Trials, Cochrane Controlled Trials Register, MEDLINE, previous reviews including cross references, abstracts, conferences, symposia proceedings, expert informants and journal handsearching in the English language. SELECTION CRITERIA: All trials using random or quasi-random patient allocation, in which thyroid hormone therapy (either treatment or prophylaxis) was compared to a control in premature infants. DATA COLLECTION AND ANALYSIS: Primary clinical outcomes included measures of neurodevelopmental outcome and mortality. Assessment of trial quality, data extraction and synthesis of data, using relative risk (RR) and weighted mean difference (WMD), were performed using standard methods of the Cochrane Collaboration and its Neonatal Review Group. MAIN RESULTS: Eight studies were identified that compared thyroid hormone treatment to control. Four randomized or quasi-randomized studies met inclusion criteria (Chowdhry 1984, Amato 1989, van Wassenaer 1997 and Vanhole 1997). All studies enrolled preterm infants < 32 weeks gestation, but used different timing, dose and duration of treatment with thyroid hormones. Three studies used thyroxine, whereas Amato 1989 used triiodothyronine. Only two studies with neurodevelopmental follow-up were of good methodology (van Wassenaer 1997 and Vanhole 1997). All studies were of small size with the largest, van Wassenaer 1997, enrolling 200 infants. A lack of comparability of data (neurodevelopmental test or timing of follow-up) prevented meta-analytic pooling of the studies for neurodevelopmental outcomes. There was no significant difference in mortality to discharge (typical relative risk 0.74, 95% CI 0.44, 1.26) in infants who received thyroid hormone treatment compared to controls. In individual studies, no significant differences were found in neurodevelopmental outcomes including risk of abnormal neurological outcome, and Bayley Mental or Psychomotor Development Indices. No data were available for the incidences of cerebral palsy or sensorineural impairment. Fraction of inspired oxygen was lower in infants receiving triiodothyronine in one small quasi-randomized study (Amato 1989), but not in infants receiving thyroxine in a randomized study (Vanhole 1997). No other differences were found to suggest a reduced severity of respiratory distress syndrome in infants receiving early thyroid hormone therapy. REVIEWER'S CONCLUSIONS: This review does not support the use of thyroid hormones in preterm infants to reduce neonatal mortality, improve neurodevelopmental outcome or to reduce the severity of respiratory distress syndrome. The a posteriori subgroup analyses of data from one study (van Wassenaer 1997) which showed benefits in infants 24-25 weeks gestation should be treated with caution. The small number of infants included in trials incorporated in this review limits the power of the meta-analysis to detect clinically important differences in neonatal outcomes. Future trials should be of sufficient size to detect clinically important differences in neurodevelopmental outcomes. They should consider enrolling those infants most likely to benefit from thyroid hormone treatment such as infants born at less than 27 weeks gestation and use thyroid hormones as treatment instead of prophylaxis.
Developmental Disabilities↗
Growth hormone secretion dynamics in a patient with ectopic growth hormone-releasing factor production.
A female patient with acromegaly, hypercalcemia, and Zollinger-Ellison syndrome was found to have a very high plasma concentration (average 2,300 pmol/liter; normal less than 50 pmol/liter) of growth hormone-releasing factor as measured by a radioimmunoassay to human pituitary growth hormone-releasing factor-1-44. The plasma concentration of growth hormone averaged 25 mIU/liter (normal less than 5 mIU/liter) and there was no rise following an intravenous 100 micrograms bolus of human pituitary growth hormone-releasing factor-1-44. Plasma growth hormone and growth hormone-releasing factor levels were unaffected by bromocriptine, insulin-induced hypoglycemia, and sleep. A long-acting somatostatin analogue lowered both the growth hormone-releasing factor and the growth hormone levels. Thyrotropin-releasing hormone stimulation and oral glucose tolerance tests produced significant increases in plasma growth hormone levels whereas the growth hormone-releasing factor level remained unchanged, suggesting that when normal somatotrophs are exposed to maximal growth hormone-releasing factor stimulation, thyrotropin-releasing hormone becomes a secretagogue of growth hormone from the pituitary. It is proposed that in the absence of a radioimmunoassay for growth hormone-releasing factor, a lack of growth hormone response to growth hormone-releasing factor in a patient with acromegaly is compatible with a source of ectopic growth hormone-releasing factor production.
Apudoma↗
Long-term growth hormone responses to nonspecific hypothalamic hormones in acromegalic patients.
Nonspecific hypothalamic hormones such as thyrotropin-releasing hormone or luteinizing hormone-releasing hormone, or both, elicited abnormal growth hormone responses in 73 of 108 (67.6%) acromegalic patients. After transsphenoidal adenomectomy, the provocative tests using these hormones were repeated in 26 patients with abnormal preoperative growth hormone responses to study variations in these responses during a 1-8-year observation period (average duration, 4 years). After surgery, 7 of the 26 patients regained normal basal growth hormone levels (less than 5 ng/mL) and manifested normal responses to the hypothalamic hormones. During the postoperative observation period, their basal growth hormone levels remained normal as did their responses to provocation with hypothalamic hormones, confirming that the adenoma had been completely resected. Eight other patients demonstrated normal growth hormone levels after surgery; however, they continued to have abnormal responses to provocation with hypothalamic hormones, suggesting the presence of residual adenomatous tissue in the gland. These patients manifested no marked increase in basal or peak growth hormone levels during the follow-up period (from less than 1 to less than 7.5 years) and they were all in clinical remission without any other treatment. Only one incompletely adenomectomized patient who had received no additional treatment experienced regrowth of the tumor. The main factor affecting the surgical results appears to be the preoperative basal growth hormone level, because abnormal growth hormone secretion ceased in all patients who had manifested preoperative levels below 45 ng/mL. Technical refinements of the operative procedure are another important factor in the postoperative outcome. Peritumoral tissue resection after simple selective adenomectomy is mandatory for better surgical results. Our studies indicate that fairly good results can be obtained without risk of the recurrence of the tumor or regrowth, when postoperative growth hormone levels are below 5 ng/mL and that the results are not affected by the postoperative growth hormone responses to provocation with hypothalamic hormones.
Acromegaly↗
Modulatory actions of luteinizing hormone-releasing hormone on electrical activity of preoptic neurons in brain slices.
Single unit activity was recorded from 378 neurons, in two preoptic nuclei rich in luteinizing hormone-releasing hormone neurons, using in vitro brain tissue slices which were prepared form either ovariectomized or ovariectomized plus estradiol-treated rats. To test possible transmitter-like actions, agents were injected into the perfusion medium. Luteinizing hormone-releasing hormone excited 46%, inhibited 7%, and evoked biphasic responses in 2% of the 250 units tested. By comparison, two other peptides, thyrotropin-releasing hormone and cholecystokinin-octapeptide sulfated were exclusively excitatory, acting on 55 and 67% of the neurons, respectively. The response to thyrotropin-releasing hormone, cholecystokinin-octapeptide sulfated, and neurotransmitters were prompt, large, and consistent from trial to trial. In contrast, responses to luteinizing hormone-releasing hormone were usually delayed, small, and variable. Responses to the agents tested were not affected by in vivo estradiol treatment. Possible modulatory actions of luteinizing hormone-releasing hormone were tested by comparing the responses of single neurons to norepinephrine and serotonin before and after an application of luteinizing hormone-releasing hormone. In 39 and 20% of the 119 neurons tested, the norepinephrine responses were potentiated and attenuated, respectively, by luteinizing hormone-releasing hormone. In 46 serotonin-responsive neurons, 28% were potentiated and 22% attenuated. These neuromodulatory actions of luteinizing hormone-releasing hormone were specific in affecting only certain responses of certain neurons, and they were not duplicated on the same neurons by thyrotropin-releasing hormone. It appears that luteinizing hormone-releasing hormone may be a neuromodulator in the preoptic area.
Action Potentials↗
A multidisciplinary approach to the study of T cell migration.
Active T cell locomotion depends on efficient repeated cycles of integrin receptor/ligand interactions mediating cell adhesion and detachment, intracellular signaling cascades orchestrating posttranslation modifications of interacting proteins, dynamic reassembly of participating cytoskeletal elements, and structural support of associated scaffolding molecules. Using an integrated approach based on novel cutting edge technologies of live cell imaging, cell transfection, proteomics, and nanotechnology, we provide here a detailed characterisation of crucial mechanisms involved in LFA-1 integrin-mediated T cell migration. Polarization and phenotypic changes associated with LFA-1-triggered T cell locomotion is largely dependent on the intact functioning of the microtubule cytoskeleton. Experiments utilizing 4-D (3-D over time) confocal live imaging of T cells, microinjected with fully functional constructs encoding protein kinase C beta (PKC-beta) isoenzyme tagged with enhanced green fluorescent protein (GFP), elucidate that LFA-1-induced activation is associated with translocation of PKC-beta to sites associated with centrosomes and tubulin cytoskeleton in locomotory T lymphocytes. We also provide here a characterization of a novel microfluidics-based multichannel platform enabling detailed analysis of leukocyte adhesion and migration under regulated shear stress conditions. Using precision machined surfaces, we demonstrate that the substrate topography can influence the motile response of the two different T cell types in different ways, and this can be quantified in terms of specified motility parameters. Finally, using an original in situ immunoprecipitation method, in which LFA-1 antibodies are utilized to induce intracellular association of proteins in the cytoskeletal/signaling complex, we demonstrate that this complex includes a number of structural and signaling proteins, which have been identified by 2-D electrophoresis and MALDI-TOF protein sequencing.
Cell Adhesion↗
Action of luteinizing hormone-releasing hormone: involvement of novel arachidonic acid metabolites.
Anterior pituitary cells were incubated in the presence of luteinizing hormone-releasing hormone and one of three inhibitors of arachidonic acid metabolism:indomethacin, an inhibitor of the cyclooxygenase system; nordihydroguaiaretic acid, an antioxidant that inhibits lipoxygenase; and icosatetraynoic acid, an acetylenic analogue of arachidonic acid that blocks all known pathways of arachidonic acid metabolism. Indomethacin was ineffective in blocking luteinizing hormone-releasing hormone-stimulated luteinizing hormone secretion. Nordihydroguaiaretic acid was only marginally capable of inhibiting luteinizing hormone-releasing hormone-stimulated luteinizing hormone secretion. Icosatetraynoic acid at 10 microM completely inhibited stimulated luteinizing hormone secretion. Addition of several epoxygenated arachidonic acid metabolites to cells in vitro resulted in secretion of luteinizing hormone equal to or greater than that induced by 10 nM luteinizing hormone-releasing hormone. The half-maximal effective dose for these compounds was approximately 50 nM. The 5,6-epoxyicosatrienoic acid was the most potent of the compounds tested. These studies suggest that luteinizing hormone-releasing hormone-stimulated luteinizing hormone release is closely coupled with the production of oxidized arachidonic acid metabolites. Moreover, one or more of the epoxygenated arachidonic acid metabolites might be a component of the cascade of reactions initiated by luteinizing hormone-releasing hormone that ultimately results in secretion of luteinizing hormone.
5,8,11,14-Eicosatetraynoic Acid↗
Plasma integrated concentration of growth hormone after recombinant human growth hormone injection. Implications for determining an optimal dose.
OBJECTIVE: To evaluate the effect of a standard dose of injected recombinant growth hormone on the integrated concentrations of growth hormone and insulin. DESIGN: Integrated concentrations were studied in patients receiving growth hormone therapy before and on the day of injection. SETTING: Pediatric endocrine clinic and diagnostic unit. PATIENTS: Twelve growth hormone-deficient patients with poor linear growth and deficient growth hormone response to provocative stimulation and/or 24-hour integrated concentration. INTERVENTION: Patients received subcutaneous injections of 0.06 mg/kg of growth hormone three times a week in the evenings at approximately 8 PM. Integrated concentrations were measured again approximately 6 months after the start of therapy at the time of a growth hormone injection. MEASUREMENTS AND RESULTS: Mean growth hormone dose administered was 2.0 +/- 0.5 mg. Integrated concentration of growth hormone was 2.2 +/- 0.9 micrograms/L before therapy. The integrated concentration of growth hormone after treatment (14.6 +/- 4.2 micrograms/L) was significantly higher than that before treatment and that of normally growing children (P < .001). After injection, peak growth hormone level was 53.7 +/- 24.1 micrograms/L; time to peak growth hormone level, 4.8 +/- 1.2 hours; constant of elimination, 0.24 +/- 0.06 per hour; half life, 3.0 +/- 0.7 hours; area under the curve, 328 +/- 85 (microgram.h)/L; clearance rate, 107.6 +/- 34.3 mL/min (3.2 +/- 0.8 mL/min per kilogram based on weight, 95.2 +/- 24.2 mL/min per meter squared based on surface area). There was no relationship between integrated concentration of growth hormone or pharmacokinetic variables after treatment and the growth response to 6 months' therapy. Integrated concentration of insulin before treatment was 19.0 +/- 10.9 mU/L, which was significantly lower than that after injection of growth hormone (33.4 +/- 9.5 mU/L; n = 9, P < .0008). CONCLUSIONS: Integrated concentrations of growth hormone after an injection of 0.06 mg/kg of growth hormone are considerably higher than spontaneous integrated concentrations of growth hormone observed in normally growing children, and associated with a rise in insulin secretion. These changes may be pertinent in patients with underlying insulin resistance or when higher doses of growth hormone are used for therapy.
Adolescent↗
Feeding-dependent depression of melanin-concentrating hormone and melanin-concentrating hormone receptor-1 expression in vagal afferent neurones.
Food intake is regulated by signals from the gastrointestinal tract. Both stimulation and inhibition of food intake may be mediated by upper gastrointestinal tract hormones, e.g. ghrelin and cholecystokinin that act at least partly via vagal afferent neurones. We now report that vagal afferent neurones in both rat and man express melanin-concentrating hormone and its receptor, melanin-concentrating hormone-1R. In nodose ganglia from rats fasted for 24 h, RT-PCR revealed the expression of both melanin-concentrating hormone and melanin-concentrating hormone-1R, whereas in ganglia from animals fed ad libitum expression was virtually undetectable. Immunohistochemical studies also revealed expression of melanin-concentrating hormone and melanin-concentrating hormone-1R in nodose ganglion neurones of fasted rats, but signals were weak in rats fed ad libitum. Melanin-concentrating hormone and melanin-concentrating hormone-1R were expressed in the same neurones, a high proportion of which also expressed the cholecystokinin-1 receptor. When fasted rats were refed, there was down-regulation of melanin-concentrating hormone and melanin-concentrating hormone-1R expression over a period of 5 h. Similar effects were produced by administration of cholecystokinin to fasted rats. The cholecystokinin-1 receptor antagonist lorglumide inhibited food-induced down-regulation of melanin-concentrating hormone and melanin-concentrating hormone-1R. We conclude that the satiety hormone cholecystokinin acts on vagal afferent neurones to inhibit expression of melanin-concentrating hormone and its receptor. Since the melanin-concentrating hormone system is associated with stimulation of food intake this effect of cholecystokinin may contribute to its action as a satiety hormone.
Afferent Pathways↗
Novel mechanisms of growth hormone regulation: growth hormone-releasing peptides and ghrelin.
Growth hormone secretion is classically modulated by two hypothalamic hormones, growth hormone-releasing hormone and somatostatin. A third pathway was proposed in the last decade, which involves the growth hormone secretagogues. Ghrelin is a novel acylated peptide which is produced mainly by the stomach. It is also synthesized in the hypothalamus and is present in several other tissues. This endogenous growth hormone secretagogue was discovered by reverse pharmacology when a group of synthetic growth hormone-releasing compounds was initially produced, leading to the isolation of an orphan receptor and, finally, to its endogenous ligand. Ghrelin binds to an active receptor to increase growth hormone release and food intake. It is still not known how hypothalamic and circulating ghrelin is involved in the control of growth hormone release. Endogenous ghrelin might act to amplify the basic pattern of growth hormone secretion, optimizing somatotroph responsiveness to growth hormone-releasing hormone. It may activate multiple interdependent intracellular pathways at the somatotroph, involving protein kinase C, protein kinase A and extracellular calcium systems. However, since ghrelin has a greater ability to release growth hormone in vivo, its main site of action is the hypothalamus. In the current review we summarize the available data on the: a) discovery of this peptide, b) mechanisms of action of growth hormone secretagogues and ghrelin and possible physiological role on growth hormone modulation, and c) regulation of growth hormone release in man after intravenous administration of these peptides.
Ghrelin↗
Three distinct thyrotropin-releasing hormone-immunoreactive axonal systems project in the median eminence-pituitary complex of the frog Rana ridibunda. Immunocytochemical evidence for co-localization of thyrotropin-releasing hormone and mesotocin in fibers innervating pars intermedia cells.
The localization of thyrotropin-releasing hormone-immunoreactive structures was investigated in the hypothalamo-hypophyseal complex of the frog, Rana ridibunda, by light and electron microscopy using the conventional indirect immunoperoxidase technique and the immuno-gold technique, respectively. The localization of mesotocin-, vasotocin- and neurophysin-immunoreactive elements was compared to that of thyrotropin-releasing hormone either by comparing homologous fields on serial sections or by staining the same section with two different antibodies. Thyrotropin-releasing hormone-immunoreactive perikarya occurred mainly in the anterobasal periventricular area and dorsal extension of the preoptic nucleus, and in the lateral zone of the infundibular nucleus. In the anterobasal preoptic nucleus, the distribution of thyrotropin-releasing hormone-immunoreactive perikarya partially overlapped that of vasotocin- and mesotocin-containing neurons; however, co-localization of thyrotropin-releasing hormone with either nonapeptide could not be detected there. In contrast, in the caudal extension of the preoptic nucleus, thyrotropin-releasing hormone- and mesotocin-like immunoreactivities were frequently co-localized in the same neurons. In the external zone of the median eminence, abundant networks of thyrotropin-releasing hormone- and vasotocin-immunoreactive nerve fibers were found in the vicinity of portal capillaries, while mesotocin-immunoreactive axons were only found in the internal zone. Using the immuno-gold technique at the electron microscopic level, three distinct thyrotropin-releasing hormone-immunoreactive systems were identified in the median eminence-neurointermediate lobe complex. (1) In the external zone of the median eminence, a conspicuous population of pericapillary endings contained 100-nm dense core vesicles immunoreactive solely for thyrotropin-releasing hormone. (2) In the neural lobe of the pituitary, thyrotropin-releasing hormone immunoreactivity occurred on secretory vesicles in a subpopulation of the mesotocinergic axons containing 160-nm secretory granules; co-localization with vasotocin was never seen. (3) In the intermediate lobe, thyrotropin-releasing hormone- and mesotocin (or neurophysin I)-immunoreactivities were systematically found in the same 120-nm dense core vesicles; these thyrotropin-releasing hormone-/mesotocin-immunoreactive axon terminals frequently made synaptic contacts with melanotropic cells. The possible modulatory effect of mesotocin on thyrotropin-releasing hormone-induced alpha-melanocyte-stimulating hormone secretion was investigated using perifused frog neurointermediate lobes. Administration of graded doses of mesotocin (from 10(-10) to 10(-5) M) did not affect the spontaneous release of alpha-melanocyte-stimulating hormone. In addition, mesotocin (10(-7) and 10(-6) M) did not modify thyrotropin-releasing hormone-evoked alpha-melanocyte-stimulating hormone release.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗