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PubMed2006

Cloning and characterization of cDNAs for hormones and/or receptors of growth hormone, insulin-like growth factor-I, thyroid hormone, and corticosteroid and the gender-, tissue-, and developmental-specific expression of their mRNA transcripts in fathead minnow (Pimephales promelas).

Growth hormone (GH), insulin-like growth factor-I (IGF-I), thyroid hormones, and corticosteroids play central roles in a wide range of body functions but, in fish, information on their interactions is limited. These axes of the endocrine system are also potential targets for disruption of signaling pathways by hormone-mimicking chemicals, but have received little study. Molecular approaches offer an effective way to help unravel these endocrine interactions but require the appropriate gene-specific assays to do so. In this study, the cDNAs for a suite of hormones and/or receptors involved in signaling for the effects of GH and IGF-I [GH, GH receptor (GHR), IGF-I, IGF-I receptor (IGF-IR)], thyroid hormones [thyroid hormone receptor alpha (TRalpha) and beta (TRbeta)], and corticosteroids [glucocorticoid receptor (GR)] were cloned from the fathead minnow (Pimephales promelas; fhm), and the tissue-, developmental-, and gender-related expression of their mRNA transcripts established. By polymerase chain reaction (PCR) strategy, we obtained full-length 1123-bp GH, 817-bp IGF-I, 1584-bp TRbeta, and 2571-bp GR cDNAs, coding for 210 amino acid (aa) GH, 161 aa IGF-I, 378 aa TRbeta, and 745 aa GR putative proteins, and partial-length 158-bp GHR, 811-bp IGF-IR, and 446-bp TRalpha cDNAs. Real-time PCR analyses revealed broad tissue expression for the target mRNAs; all targets were expressed in brain, pituitary, gill, liver, gonad, intestine, and muscle, with the exception of GH that was expressed only in the pituitary and gonad. Expression patterns in both juvenile and adult fhm were complex, with both temporal-, tissue-, and sex-specific characteristics. For example, hepatic expressions of GHR, IGF-I, and IGF-IR were far higher in males than in females, possibly reflecting the sex-related dimorphism in growth that occurs in this species, and TRalpha and TRbeta showed divergent expression patterns during development (where TRbeta predominated) and in adult tissues implying some distinct roles for the two TR subtypes.

Adrenal Cortex Hormones↗
PubMed1982

Growth hormone response to thyrotropin-releasing hormone in liver cirrhosis: unique alteration in anterior pituitary responsiveness to hypothalamic hormones.

Patients with chronic liver diseases were evaluated for: 1) the ability of somatostatin to affect the thyrotropin-releasing hormone (TRH) induced growth hormone (GH) rise; 2) the competence of luteinizing-hormone releasing hormone (LH-RH) to release GH; 3) the non-specific releasing effect of TRH and LH-RH on other anterior pituitary (AP) hormones. In 6 patients, infusion of somatostatin (100 micrograms iv bolus + 375 micrograms i.v. infusion) completely abolished the TRH (400 micrograms i.v.)-induced GH rise; in none of 12 patients, of whom 7 were GH-responders to TRH, did LH-RH (100 micrograms i.v.) cause release of GH; 4) finally, LH-RH (12 patients) did not increase plasma prolactin (PRL) and TRH (7 patients) did not evoke a non-specific release of gonadotropins. It is concluded that: 1) abnormal GH-responsiveness to TRH is the unique alteration in AP responsiveness to hypothalamic hormones present in liver cirrhosis; 2) the mechanism(s) subserving the altered GH response to TRH is different from that underlying the TRH-induced GH rise present in another pathologic state i.e. acromegaly, a condition in which the effect of TRH escapes somatostatin suppression and LH-RH evokes GH and PRL release.

Adult↗
PubMed2006

Growth hormone-releasing hormone and corticotropin-releasing hormone enhance non-rapid-eye-movement sleep after sleep deprivation.

The neuropeptides growth hormone (GH)-releasing hormone (GHRH) and corticotropin-releasing hormone (CRH) regulate sleep and nocturnal hormone secretion in a reciprocal fashion, at least in males. GHRH promotes sleep and GH and inhibits hypothalamo-pituitary-adrenocortical (HPA) hormones. CRH exerts opposite effects. In women, a sexual dimorphism was found because GHRH impairs sleep and stimulates HPA hormones. Sleep deprivation (SD) is the most powerful stimulus for inducing sleep. Studies in rodents show a key role of GHRH in sleep promotion after SD. The effects of GHRH and CRH on sleep-endocrine activity during the recovery night after SD are unknown. We compared sleep EEG, GH, and cortisol secretion between nights before and after 40 h of SD in 48 normal women and men aged 19-67 yr. During the recovery night, GHRH, CRH, or placebo were injected repetitively. After placebo during the recovery night, non-rapid-eye-movement sleep (NREMS) and rapid-eye-movement sleep (REMS) increased and wakefulness decreased compared with the baseline night. After GHRH, the increase of NREMS and the decrease of wakefulness were more distinct than after placebo. Also, after CRH, NREMS increased higher than after placebo, and a positive correlation was found between age and the baseline-related increase of slow-wave sleep. REMS increased after placebo and after GHRH, but not after CRH. EEG spectral analysis showed increases in the lower frequencies and decreases in the higher frequencies during NREMS after each of the treatments. Cortisol and GH did not differ between baseline and recovery nights after placebo. After GHRH, GH increased and cortisol decreased. Cortisol increased after CRH. No sex differences were found in these changes. Our data suggest that GHRH and CRH augment NREMS promotion after SD. Marked differences appear to exist in peptidergic sleep regulation between spontaneous and recovery sleep.

Adult↗
PubMed1988

Dose-related inhibition of acute luteinizing hormone response during luteinizing hormone-releasing hormone agonist treatment for uterine leiomyoma.

Twenty-six women with uterine leiomyoma were treated for 6 months with subcutaneous injections of the luteinizing hormone-releasing hormone agonist buserelin. Eight women received 200 micrograms daily, eight women received 350 micrograms daily, and 10 women after initial administration of 200 micrograms every 8 hours for 7 days, 500 micrograms of buserelin was administered daily. After 1, 3, and 6 months of treatment, serum luteinizing hormone levels were measured before and 4 and 8 hours after the administration of buserelin. The area under the curve for acute luteinizing-hormone response was then individually calculated. The inhibition of acute luteinizing hormone response during luteinizing hormone-releasing hormone agonist treatment was proportional to the dosage used and remained constant during the treatment period.

Adult↗
PubMed1995

Treatment of growth hormone-deficient adults with recombinant human growth hormone increases the concentration of growth hormone in the cerebrospinal fluid and affects neurotransmitters.

In a double-blind, placebo-controlled trial, the effects of recombinant human growth hormone were studied on cerebrospinal fluid concentrations of growth hormone, insulin-like growth factor 1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3), monoamine metabolites, neuropeptides and endogenous opioid peptides. Twenty patients, 10 patients in each of 2 groups, with adult-onset, growth hormone deficiency were treated for 1 month with recombinant human growth hormone (0.25 U/kg/week) or placebo. All the patients received the appropriate thyroid, adrenal and gonadal hormone replacement. In cerebrospinal fluid, the mean concentration of growth hormone increased from 13.3 +/- 4.4 to 149.3 +/- 22.2 muU/l (p = 0.002), during recombinant human growth hormone treatment. The cerebrospinal fluid IGF-I concentration increased from 0.67 +/- 0.04 to 0.99 +/- 0.10 micrograms/l (p = 0.005) and the IGFBP-3 concentration rose from 13.4 +/- 1.25 to 17.5 +/- 1.83 micrograms/l (p = 0.002). The dopamine metabolite homovanillic acid decreased from 282.1 +/- 36.0 to 234.3 +/- 26.5 nmol/l (p = 0.02) and the vasoactive intestinal peptide decreased from 4.1 +/- 0.6 to 3.7 +/- 0.4 pmol/l (p = 0.03). Cerebrospinal fluid immunoreactive beta-endorphin increased from 24.4 +/- 1.8 to 29.9 +/- 2.1 pmol/l (p = 0.002). There were no significant changes compared to baseline in the cerebrospinal fluid concentrations of enkephalins, dynorphin A, the norepinephrine metabolite 3-methoxy-4-hydroxyphenyl-ethyleneglycol, the serotonin metabolite 5-hydroxyindoleacetic acid, gamma-aminobutyric acid, somatostatin or corticotropin-releasing factor.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Potential use of analogs of luteinizing hormone-releasing hormones in the treatment of hormone-sensitive neoplasms.

New approaches to the therapy for some endocrine-dependent tumors with analogs of hypothalamic hormones are being developed on the basis of experimental studies in animal models. Analogs of luteinizing hormone-releasing hormones (LH-RH) may open new vistas for the treatment of some hormone-dependent carcinomas. It has been clearly demonstrated that both agonistic and antagonistic analogs of LH-RH can inhibit the growth of rat prostate tumors. A successful treatment of androgen-dependent prostate cancer with agonistic analogs of D-Trp6-LH-RH, D-Ser(But)6des-Gly-NH2(10)-LH-RH ethylamide, and D-Leu6-des-Gly-NH2(10)-LH-RH ethylamide has been documented in several hundred patients. The data accumulated so far from clinical trials suggest that LH-RH agonists can be used as an effective endocrine therapy for prostate carcinoma, therapy avoiding the side effects of estrogen and the psychologic impact of castration. Experimental animal studies and some clinical trials suggest that LH-RH agonists and/or antagonists might also be useful in the treatment of breast cancer. The results of experiments with various hypothalamic analogs in animal models of chondrosarcomas, osteosarcomas, and other tumors appear to be encouraging, but the potential clinical efficacy of LH-RH analogs in the treatment of human hormone-sensitive cancers other than breast and prostate remains to be investigated. The approach to treatment of hormone-dependent tumors based on analogs of hypothalamic hormones might become a useful addition to conventional methods for cancer therapy.

Animals↗
PubMed1977

Lack of effect of thyroid hormones on the growth hormone response to thyrotropin-releasing hormone in acromegaly.

Serum growth hormone (GH) responses to thyrotropin-releasing hormone (TRH) were evaluated in 14 patients with acromegaly following treatment with thyroid hormones. After an initial TRH test, seven patients received L-triiodothyronine, 100 mug daily for seven days; the GH response to TRH was not significantly altered by this treatment. Similar findings were noted in two acromegalic subjects who were tested with TRH before and after longer periods of administration of L-thyroxine. Four of five additional subjects with acromegaly who had received replacement doses of thyroid hormones for an average of 6.6 yr demonstrated GH responses to TRH which were similar to those seen in subjects not receiving thyroid hormones. Acute or long-term administration of replacement doses of thyroid hormones seems to have minimal effect on the GH response to TRH in acromegaly.

Acromegaly↗
PubMed1992

Corticotropin-releasing hormone inhibition of paradoxical growth hormone response to thyrotropin-releasing hormone in insulin-dependent diabetics.

A paradoxical growth hormone (GH) response to thyrotropin-releasing hormone (TRH) has been observed in type 1 diabetic patients and was hypothetically attributed to a reduced hypothalamic somatostatin tone. We have previously reported that corticotropin-releasing hormone (CRH) inhibits GH response to growth hormone-releasing hormone (GHRH) in normal subjects, possibly by an increased release of somatostatin. To study the effect of CRH on anomalous GH response to TRH, we tested with TRH (200 micrograms intravenously [IV]) and CRH (100 micrograms IV) + TRH (200 micrograms IV) 13 patients (six males and seven women) affected by insulin-dependent diabetes mellitus. A paradoxical GH response to TRH was observed in seven of 13 patients, one man and six women. In these subjects, the simultaneous administration of CRH and TRH significantly reduced the GH response to TRH, as assessed by both the maximal GH mean peak +/- SE (2.18 +/- 0.67 v 9.2 +/- 1.26 micrograms/L, P less than 0.005) and the area under the curve (AUC) +/- SE (187 +/- 32 v 567 +/- 35 micrograms.min/L, P less than .001). CRH had no effect on TRH-induced thyroid-stimulating hormone (TSH) release. Our data demonstrate that the paradoxical GH response to TRH in patients with type 1 diabetes mellitus is blocked by CRH administration. This CRH action may be due to an enhanced somatostatin release. Our data also show that exogenous CRH has no effect on TSH response to TRH, thus suggesting the existence of separate pathways in the neuroregulation of GH and TSH secretion.

Adult↗
PubMed2005

Effect of metformin on the growth hormone response to growth hormone-releasing hormone in obese women with polycystic ovary syndrome.

OBJECTIVE: Obese women with polycystic ovary syndrome (PCOS) show a marked growth hormone (GH) hyporesponsiveness to several stimuli. We aimed to evaluate the impact of insulin metabolism on the GH secretion impairment in these subjects in relation to food ingestion. DESIGN: Prospective clinical study. SETTING: Academic research center. PATIENT(S): Nine obese women with PCOS. INTERVENTION(S): Metformin (1,500 mg/daily) was administered for three months. The study protocol, which was performed before and after therapy, included hormonal and lipid assays, oral glucose tolerance test (75 g), euglycemic hyperinsulinemic clamp, and growth hormone-releasing hormone (GHRH) test (50 microg/ev), both on fasting and after a standard meal. MAIN OUTCOME MEASURE(S): Growth hormone response to GHRH (expressed as the area under the curve) in different experimental conditions. RESULT(S): The preprandial GH response to GHRH was not modified by the therapy, whereas a significant increase (P<.05) occurred in the postprandial GH secretion, thus resembling the response of obese normal persons. This change was accompanied by a trend towards improvement, though not statistically significant, of all the evaluated glycoinsulinemic parameters. A significant reduction in cholesterol (P<.01) and androstenedione (P<.05) and an increase in sex hormone-binding globulin (P<.05) were also achieved. CONCLUSION(S): These data suggest that metformin is able to affect GH secretion in obese women with PCOS, even with minimal metabolic modifications.

Adolescent↗
PubMed1985

Effect of aromatase inhibition by delta 1-testolactone on basal and luteinizing hormone-releasing hormone-stimulated pituitary and gonadal hormonal function in oligospermic men.

Aromatase inhibition by delta 1-testolactone (TL), 500 mg twice daily for 4 weeks, in nine patients with idiopathic oligospermia lowered circulating estradiol (E2) levels by about 30%, enhanced the secretion of follicle-stimulating hormone (+ 30%), 17-hydroxyprogesterone (17-OHP) (+ 40%), and testosterone (T) (+ 30%), but did not affect serum luteinizing hormone levels. Despite E2 lowering, there was an accumulation of 17-OHP over T, suggesting 17, 20-lyase inhibition. Unexpectedly, administration of TL almost completely deleted the T response to continuous luteinizing hormone-releasing hormone infusion present before TL therapy, despite similar gonadotropin release. Because the 17-OHP response to the luteinizing hormone-releasing hormone infusion was even higher during therapy, the 17,20-lyase lesion seemed aggravated despite substantial reduction of E2 levels. Although the present data suggest that estrogens play a less dominant role in the origin of the late steroidogenetic lesion than previously assumed, the suggestion also arises that TL per se, in addition to its antiestrogenic action, exerts an inhibiting effect on the 17,20-lyase locus, which may obscure the beneficial effect of reducing E2.

Adult↗
PubMed2002

Pituitary effects of steroid hormones on secretion of follicle-stimulating hormone and luteinizing hormone.

Steroid hormones have a profound influence on the secretion of the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH). These effects can occur as a result of steroid hormones modifying the secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus, or a direct effect of steroid hormones on gonadotropin secreting cells in the anterior pituitary gland. With respect to the latter, we have shown that estradiol increases pituitary sensitivity to GnRH by stimulating an increase in expression of the gene encoding the GnRH receptor. Since an estrogen response element (ERE) has not been identified in the GnRH receptor gene, this effect appears to be mediated by estradiol stimulating production of a yet to be identified factor that in turn enhances expression of the GnRH receptor gene. However, the importance of estradiol for enhancing pituitary sensitivity to GnRH during the periovulatory period is questioned because an increase in mRNA for the GnRH receptor precedes the pre-ovulatory rise in circulating concentrations of estradiol. In fact, it appears that the enhanced pituitary sensitivity during the periovulatory period may occur as a result of a decrease in concentrations of progesterone rather than due to an increase in concentrations of estradiol. Estradiol also is capable of altering secretion of FSH and LH in the absence of GnRH. In a recent study utilizing cultured pituitary cells from anestrous ewes, we demonstrated that estradiol induced a dose-dependent increase in secretion of LH, but resulted in a dose-dependent decrease in the secretion of FSH. We hypothesized that the discordant effects on secretion of LH and FSH might arise from estradiol altering the production of some of the intrapituitary factors involved in synthesis and secretion of FSH. To examine this hypothesis, we measured amounts of mRNA for activin B (a factor known to stimulate synthesis of FSH) and follistatin (an activin-binding protein). We found no change in the mRNA for follistatin after treatment of pituitary cells with estradiol, but noted a decrease in the amount of mRNA for activin B. Thus, the inhibitory effect of estradiol on secretion of FSH appears to be mediated by its ability to suppress the expression of the gene encoding activin.

Animals↗
PubMed1996

Divergence between growth hormone responses to insulin-induced hypoglycaemia and growth hormone-releasing hormone in patients with non-functioning pituitary macroadenomas and hyperprolactinaemia.

OBJECTIVE: The GH responses to the insulin tolerance test (ITT) and growth hormone-releasing hormone (GHRH) may yield different results in patients with pituitary lesions. The GH responses to these stimuli were compared in patients with untreated non-functioning pituitary macroadenomas, who represent an important cause of GH deficiency. DESIGN: Analysis of peak GH to ITT and to 100 micrograms GHRH in relation to an elevated PRL level (> 200 mIU/l for males and > 600 mIU/l for females) as an indication of hypothalamic-pituitary dysregulation, as well as in relation to other anterior pituitary hormone deficiencies. A peak GH < 5 micrograms/l in either test indicated GH deficiency. PATIENTS: Twenty females and 14 males (median age 52 (23-77) years) evaluated preoperatively in a university hospital setting. RESULTS: In the whole group the median peak GH to GHRH (3.6 (0.9-26.3) micrograms/l) was higher than to ITT (1.6 (0.2-7.8) micrograms/l, P < 0.001). This difference was seen only in 19 patients with concomitant hyperprolactinaemia (P < 0.001). When hyperprolactinaemia was present, an insufficient GH peak was demonstrated by ITT in 16 cases and by GHRH stimulation in 7 cases (P < 0.01). The frequency of an insufficient GH peak by ITT (13 cases) and by GHRH (14 cases) was similar in the normoprolactinaemic patients. In addition, 9 of 10 patients with an impaired response to ITT and a normal response to GHRH were hyperprolactinaemic compared to 7 of 19 patients with GH deficiency as assessed by both stimuli (P < 0.02). Peak GH to ITT was lower in 24 patients with, compared to 10 patients without, other hormonal deficiencies (1.4 (0.2-5.6) vs 3.0 (1.0-7.8) micrograms/l, P < 0.02), but was not related to elevated PRL. In contrast, GHRH-stimulated GH was higher in hyperprolactinaemic than in normoprolactinaemic patients (5.9 (1.6-26.3) vs 2.9 (0.9-5.4) micrograms/l, P < 0.001) and was not related to the presence of other pituitary hormone deficiencies. Analysis of covariance confirmed that peak GH to ITT was negatively associated with the presence of other pituitary hormone deficiencies (P < 0.01), whereas peak GH to GHRH was positively related to an elevated PRL level (P < 0.02). Basal GH was positively correlated with PRL (R(s) = 0.36, P < 0.05). CONCLUSIONS: This study demonstrates that ITT and GHRH tests cannot be used interchangeably in diagnosing GH deficiency in patients with non-functioning pituitary macroadenoma and hyperprolactinaemia. If the ITT is considered to be the reference test, GH deficiency as assessed by GHRH can be missed in patients with hyperprolactinaemia. This disparity is probably due to a different mechanism of action of these stimuli. Hyperprolactinaemia may be associated with a diminished somatostatin tone, leading to a higher basal and GHRH-stimulated GH, without having an effect on peak GH to ITT.

Adenoma↗
PubMedDate not supplied

[Behavior of growth hormone after stimulation with growth hormone releasing hormone (GHRH) in children with disorders of the hypothalamo-hypophyseal axis and girls with Turner syndrome].

BACKGROUND: To investigate the hypothalamic pituitary axis in children with various growth disorders stimulation tests with growth hormone releasing hormone (GHRH) were performed and compared to pharmacological stimulation tests. PATIENTS: 103 subjects were studied-15 healthy volunteers, 20 patients with isolated growth hormone deficiency (IGHD), 16 patients with multiple pituitary hormone deficiency (MPHD), 17 children with organic growth hormone deficiency (OGHD) and 35 Turner patients. METHODS: 1 microgram/kg GHRH was administered iv, blood samples were drawn before GHRH and after 5, 15, 30, 45, 60 and 90 minutes. In 53 patients a second GHRH-test was done after repeated GHRH injections (7 times 1 microgram/kg GHRH every 3 hours). RESULTS: In the group of healthy probands we found wide variations of stimulated growth hormone (GH) levels. In 7 of the 20 patients with IGHD the stimulated GH level exceeded 10 ng/ml in one of the two GHRH-tests. The maximal GH response to the second GHRH-test (8.3 +/- 6.8 ng/ml) was significantly higher (p < or = 0.025) than after the first GHRH-test (5.0 +/- 4.0 ng/ml). In patients with MPHD stimulated GH values were significantly lower than in patients with IGHD (p < or = 0.005). GHRH stimulation tests in OWHM patients did not differ from the results in children with IGHD. The GHRH induced GH response in girls with Turner syndrome was significantly lower than in the healthy volunteers (p < or = 0.025). Basal (p < or = 0.05) and GHRH stimulated GH levels (p < 0.02) were lower after estrogen administration. CONCLUSIONS: Pituitary GH secretion could be activated by repeated stimulation with GHRH (priming) in children with hypothalamic GH deficiency. Only in the patients with MPHD a correlation could be found between the result of the GHRH-stimulation and one pharmacological GH test. In children with OGHD the radiation dose was negatively correlated to the maximal GH concentrations after L-Dopa stimulation. Basal and GHRH stimulated GH levels in Turner syndrome were lower after estrogen administration.

Adolescent↗
PubMed1984

Responses to analogues of growth hormone-releasing hormone in normal subjects, and in growth-hormone deficient children and young adults.

Three analogues of growth hormone-releasing hormone (GHRH) have been compared in normal subjects. GHRH(1-29)NH2 is equipotent to GHRH(1-40); increasing doses from 10-200 micrograms per subject augments the duration of stimulated growth hormone (GH) release, but the peak serum GH shows only a poor correlation with dose. The derivative D-Ala2-GHRH(1-29)NH2 is no more potent than the unsubstituted GHRH(1-29)NH2. In 20 children and young adults with growth hormone deficiency by conventional criteria, eight showed normal or only slightly subnormal peak serum GH responses to GHRH(1-40) or GHRH(1-29)NH2. These included two patients with tumours of the hypothalamus, as well as six with idiopathic isolated growth hormone deficiency or panhypopituitarism. A poor response to GHRH was generally seen in patients on long-term GH therapy. Priming with GHRH, in either a single bolus or a continuous infusion, did not increase the GH response to GHRH. It is concluded that GHRH(1-29)NH2 is a useful analogue in the testing of GH reserve in patients with growth hormone deficiency, and has considerable potential for long-term therapy.

Adolescent↗
PubMed1990

Pathophysiology of pulsatile and copulsatile release of thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, and alpha-subunit.

Under physiological conditions, TSH, LH, FSH, and alpha-subunit are released in discrete pulses. To further characterize their neuroregulation and to investigate possible copulsatile secretion of these glycoprotein hormones, we studied the 24-h pulse profiles of all four hormones in each of four subject groups: young men, young women, postmenopausal women, and subjects with untreated primary hypothyroidism. Gonadotropin pulse properties in euthyroid men and women were similar to those previously reported, and hypothyroid subjects had normal gonadotropin pulse patterns. TSH release was pulsatile in all groups; hypothyroid subjects had increased pulse amplitude, but loss of the usual nocturnal increases in pulse amplitude. alpha-Subunit concentrations were pulsatile in all groups, with minimal circadian variation; postmenopausal and hypothyroid subjects had increased alpha-subunit pulse amplitude. We then tested pulse concordance among the four simultaneous hormone series. alpha-Subunit and the gonadotropins were significantly coreleased (triple coincidence), suggesting that all three hormones are closely linked to processes that regulate GnRH secretion. alpha-Subunit bursts were also significantly coincident with those of TSH in men, postmenopausal women, and hypothyroid subjects. Interestingly, TSH pulses were significantly concordant with those of LH and FSH, and all four hormones were significantly concordant in men, postmenopausal women, and hypothyroid subjects. In conclusion, the present findings imply that an underlying unified signal coordinates pulsatile hormone secretion from both gonadotrophs and thyrotrophs.

Adult↗
PubMed2006

Multihormonal resistance to parathyroid hormone, thyroid stimulating hormone, and other hormonal and neurosensory stimuli in patients with pseudohypoparathyroidism.

In patients with pseudohypoparathyroidism, hormonal resistance first affects parathyroid hormone (PTH), which leads to calcipenia, a decrease in renal vitamin D activation, and a tendency to bone receptor remodeling. However, because G proteins are ubiquitously distributed, multiple hormonal resistance occurs in pseudohypoparathyroidism type Ia and type Ic, impairing responses to other calciotropic hormones (PTHrP, calcitonin), TSH, and also pituitary and hypothalamic hormones, and to neurosensory stimuli. The diversity of multihormonal resistance contributes to the various phenotypes of the disease. Some clinical discomfort and medical consequences of the disease can be treated or prevented with hormone supplementation or modulation.

Hearing↗
PubMed1990

Inhibition of endopeptidase 24.15 greatly increases the release of luteinizing hormone and follicle stimulating hormone in response to luteinizing hormone/releasing hormone.

Inhibitors of endopeptidase (EP) 24.15, an enzyme cleaving the Tyr5-Gly6 bond of LHRH, greatly increase the half-life of i.v. or i.c.v. administered luteinizing hormone-releasing hormone (LHRH) (Lasdun et al., J. Pharmacol. Exp. Ther. 251: 439-447, 1989). Concentrations of plasma luteinizing hormone (LH) and follicle stimulating hormone (FSH) were measured in rats after i.c.v. and i.v. administration of LHRH alone or in conjunction with inhibitors of EP 24.15. In animals treated with two potent EP 24.15 inhibitors, i.v. and i.c.v. LHRH injections induced a much greater and longer-lasting increase of plasma LH and FSH concentrations than in controls Two and 4 hr after administration of the inhibitors and LHRH, hormone concentrations were one order of magnitude greater than in controls. The magnitudes and durations of the increases were similar to those after administration of [D-Trp6]-LHRH or [D-Leu6, Des-Gly-NH2(10)]-LHRH ethylamide, two "superactive" analogs of LHRH, which are resistant to degradation by EP 24.15, due to the presence of a D-amino acid in position 6. It is concluded that LHRH degradation by EP 24.15 limits the magnitude and duration of the response of the pituitary to LHRH, and that increases in plasma LH and FSH similar to those obtained after administration of superactive analogs can be also obtained with the natural hormone, provided that its degradation is prevented by EP 24.15 inhibitors. Accordingly, the increased in vivo activity of the superactive LHRH analogs can be largely attributed to their resistance to degradation by EP 24.15.

Animals↗
PubMed1989

Plasma growth hormone responses to growth hormone-releasing hormone in children of short stature.

Synthetic GHRH-(1-44)NH2 was administered as an i.v. bolus dose of 2 micrograms/kg to 14 normal short children and 20 children with growth hormone deficiency. In normal short children, mean plasma GH levels reached a peak value of 54.8 mU/L at 30 min; in children with growth hormone deficiency, mean plasma GH levels reached a peak value of 18.6 mU/L at 45 min. In the majority of normal short children, the peak GH values after GHRH administration were greater than GH values after clonidine. The 20 children with growth hormone deficiency had a lower median maximum plasma GH concentration than the 14 normal short children (median 17.1 mU/L vs 49.6 mU/L). There was no significant difference in the distribution of peak GH response time between these two groups. Among 19 children with idiopathic growth hormone deficiency, 47% had a peak GH above 20 mU/L after GHRH. In these children, GHRH administration provided information on the putative hypothalamic etiology of their growth hormone deficiency. These results confirm that GHRH testing is useful for differentiating hypothalamic from pituitary growth hormone deficiency and may be of potential therapeutic value.

Adolescent↗