scholarly journals Evidence for a negative feedback in the control of eel growth hormone by thyroid hormones

2002 ◽  
Vol 175 (3) ◽  
pp. 605-613 ◽  
Author(s):  
K Rousseau ◽  
N Le Belle ◽  
M Sbaihi ◽  
J Marchelidon ◽  
M Schmitz ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Thyroid Hormones ◽  
Messenger Rna ◽  
Cdna Probe ◽  
Present Species ◽  
Species Variation ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Dependent Manner

The regulation of growth hormone (GH) by thyroid hormones (THs) has been shown to present species variation. We investigated the regulation of GH in the eel, a representative of an ancient group of teleosts. In vivo administration of triiodothyronine (T(3)) or thyroxine (T(4)) significantly reduced pituitary and serum GH levels, as measured by homologous RIA. In order to investigate the ability of THs to regulate GH production directly at the pituitary level, we used a long-term, serum-free primary culture of eel pituitary cells. Both T(3) and T(4) inhibited GH release in a concentration-dependent manner, producing up to 50% inhibition at 10 nM, with an ED(50) of <0.2 nM, within the range of their physiological circulating levels. Other hormones also acting via the nuclear receptor superfamily, such as sex steroids (testosterone, estradiol and progesterone) and corticosteroid (cortisol), had no effect on GH release in vitro, underlining the specificity of the regulatory effect of THs on GH. Measurement of both GH release and cellular content for calculation of GH production in vitro indicated that THs not only inhibited GH release but also GH synthesis. Dot-blot assay of GH messenger RNA (mRNA) using an homologous eel cDNA probe showed a decrease in GH mRNA levels in cells cultured in the presence of T(3), as compared with control cells. This demonstrated that the inhibition of T(3) on GH synthesis was mediated by a decrease in GH mRNA steady state levels. In conclusion, we demonstrate inhibitory regulation of eel GH synthesis and release by THs, exerted directly at the pituitary level. These data contrast with the rat, where THs are known to have a stimulatory effect and suggest that the pattern observed here in an early vertebrate and also found in birds, reptiles and some mammals including humans, may represent an ancestral and more generalized vertebrate pattern of TH regulation of pituitary GH.

Influence of catecholamines, prostaglandins and thyroid hormones on growth hormone secretion by chicken pituitary cells in vitro

1990 ◽  
Vol 7 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Dan J. Donoghue ◽  
Frank M. Perez ◽  
Bruce S.A. Diamante ◽  
Sasha Malamed ◽  
Colin G. Scanes
Keyword(s):  
Growth Hormone ◽  
Thyroid Hormones ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Pituitary Cells

scholarly journals Differential Effects of Gonadotropin-Releasing Hormone (GnRH) Pulse Frequency on Gonadotropin Subunit and GnRH Receptor Messenger Ribonucleic Acid Levels in Vitro*

Endocrinology ◽  
1997 ◽  
Vol 138 (3) ◽  
pp. 1224-1231 ◽  
Author(s):  
Ursula B. Kaiser ◽  
Andrzej Jakubowiak ◽  
Anna Steinberger ◽  
William W. Chin
Keyword(s):  
Gene Expression ◽  
Messenger Rna ◽  
Pulse Frequency ◽  
Gnrh Receptor ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Subunit Gene ◽  
Differential Effects ◽  
Messenger Ribonucleic Acid

Abstract The hypothalamic hormone, GnRH, is released and transported to the anterior pituitary in a pulsatile manner, where it binds to specific high-affinity receptors and regulates gonadotropin biosynthesis and secretion. The frequency of GnRH pulses changes under various physiological conditions, and varying GnRH pulse frequencies have been shown to regulate differentially the secretion of LH and FSH and the expression of the gonadotropin α, LHβ, and FSHβ subunit genes in vivo. We demonstrate differential effects of varying GnRH pulse frequency in vitro in superfused primary monolayer cultures of rat pituitary cells. Cells were treated with 10 nm GnRH pulses for 24 h at a frequency of every 0.5, 1, 2, or 4 h. α, LHβ, and FSHβ messenger RNA (mRNA) levels were increased by GnRH at all pulse frequencies. α and LHβ mRNA levels and LH secretion were stimulated to the greatest extent at a GnRH pulse frequency of every 30 min, whereas FSHβ mRNA levels and FSH secretion were stimulated maximally at a lower GnRH pulse frequency, every 2 h. GnRH receptor (GnRHR) mRNA levels also were increased by GnRH at all pulse frequencies and were stimulated maximally at a GnRH pulse frequency of every 30 min. Similar results were obtained when the dose of each pulse of GnRH was adjusted to maintain a constant total cumulative dose of GnRH over 24 h. These data show that gonadotropin subunit gene expression is regulated differentially by varying GnRH pulse frequencies in vitro, suggesting that the differential effects of varying GnRH pulse frequencies on gonadotropin subunit gene expression occur directly at the level of the pituitary. The pattern of regulation of GnRHR mRNA levels correlated with that of α and LHβ but was different from that of FSHβ. This suggests that α and LHβ mRNA levels are maximally stimulated when GnRHR levels are relatively high, whereas FSHβ mRNA levels are maximally stimulated at lower levels of GnRHR expression, and that the mechanism for differential regulation of the gonadotropins by varying pulse frequencies of GnRH may involve levels of GnRHR. Furthermore, these data suggest that the mechanisms whereby varying GnRH pulse frequencies stimulate α, LHβ, and GnRHR gene expression are similar, whereas the stimulation of FSHβ mRNA levels may be different.

GRF increases release of growth hormone and arachidonate from anterior pituitary cells

1985 ◽  
Vol 248 (4) ◽  
pp. E438-E442
Author(s):  
A. M. Judd ◽  
K. Koike ◽  
R. M. MacLeod
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Concentration Dependent Manner ◽  
Anterior Pituitary Cells ◽  
Arachidonate Release

Arachidonate and its metabolites increase growth hormone release in vitro. A study was designed to determine whether arachidonate release from anterior pituitary cells is modified by growth hormone-releasing factor (GRF) or somatostatin (SRIF). Cultured pituitary cells were incubated with [3H]arachidonate to esterify the long-chain fatty acid into cellular lipids. The cells were extensively washed with medium containing no [3H]arachidonate and then incubated with GRF and/or SRIF for 30 min. The incubation medium was then extracted with ethyl acetate, and following thin-layer chromatographic separation, the radioactivity in the [3H]arachidonate band was measured. GRF in a concentration-dependent manner (1-30 nM) stimulated growth hormone and arachidonate release, whereas SRIF (100 nM) blocked the GRF-induced increase of growth hormone and arachidonate release. The effects of GRF on growth hormone and arachidonate were evident at time intervals as brief as 5 min. These findings support the hypothesis that arachidonate may play a role in the GRF-induced growth hormone release.

Biological activity of a growth hormone-releasing factor secreted by a human tumor

1983 ◽  
Vol 244 (4) ◽  
pp. E346-E353
Author(s):  
M. J. Cronin ◽  
A. D. Rogol ◽  
R. M. MacLeod ◽  
D. A. Keefer ◽  
I. S. Login ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Cyclic Amp ◽  
Islet Cell Tumor ◽  
Hormone Secretion ◽  
Human Tumor ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
Luteinizing Hormone Secretion ◽  
Pancreatic Islet Cell

A substance released by a pancreatic islet cell tumor induced signs and symptoms of acromegaly in a young woman. The culture medium in which the tumor was placed after resection was added to rat anterior pituitary cells and incubated in vitro. Both newly synthesized and total rat growth hormone (GH) release as well as cellular cyclic AMP accumulation were stimulated in a dose-dependent manner by the tumor medium. Coincubation with somatostatin blocked these effects. The increase of cyclic AMP preceded the enhanced GH release, indicating that cyclic AMP may be a second messenger for the tumor factor(s). Neither prolactin nor luteinizing hormone secretion was affected by the tumor medium. When measured by a perfused cell column apparatus, there was a rapid and dramatic release of GH by the dispersed rat pituitary cells during a 2.5-, 10-, and 40-min pulse of tumor medium; both the onset and termination of the GH response reached maximal or control values, respectively, within 5 min. Pretreatment of the tumor medium with pepsin markedly attenuated the tumor medium activity, indicating the peptide nature of the factor(s). Finally, ultrastructural analysis indicated that the somatotrophs were degranulated by the tumor medium, whereas there was no similar effect apparent on the mammotrophs. Whether this tumor polypeptide is identical to native hypothalamic GH-releasing hormone remains to be proved.

Cyclic adenosine nucleotides and growth hormone-releasing factor increase cytosolic growth hormone messenger RNA levels in cultured rat pituitary cells

1986 ◽  
Vol 110 (1) ◽  
pp. 51-57 ◽  
Author(s):  
R. N. Clayton ◽  
L. C. Bailey ◽  
S. D. Abbot ◽  
A. Detta ◽  
K. Docherty
Keyword(s):  
Growth Hormone ◽  
Gene Transcription ◽  
Messenger Rna ◽  
Primary Cultures ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Rat Pituitary ◽  
Cdna Hybridization ◽  
Adenosine Nucleotides ◽  
Rat Pituitary Cells

ABSTRACT The cellular mechanisms involved in GH biosynthesis have been investigated by the measurement of steady-state levels of cytosolic GH messenger RNA (mRNA) in primary cultures of rat pituitary cells using an RNA–complementary DNA (cDNA) hybridization assay. Growth hormone mRNA–cDNA hybridization increased in a linear manner with increasing cytosol concentration. Cellular GH mRNA levels rose by an average of 2·4-fold (range, 1·6–3·3; n = five experiments) after exposure to GH-ieleasing factor (GRF(1–40); 10 nmol/l) for 3 days. Treatment with GRF increased the release of GH into the culture medium, and depleted the cellular GH content by 40%. Total GH (in the medium plus cells) after GRF treatment increased by between 1·5- and 3·8-fold, a magnitude similar to the increase in GH mRNA levels. Treatment of cells with dibutyryl adenosine 3′:5′-cyclic monophosphate (1 mmol/l) or forskolin (5 μmol/l) increased the levels of cytosolic GH mRNA by between 1·6- and 4·7-fold. These agents increased GH release into the medium, depleted cellular GH content and increased total GH in the system to the same extent as GRF (10 nmol/l). These data demonstrate that cyclic adenosine nucleotides may mediate the GRF induction of GH gene transcription. In addition, we have shown that increases in the levels of cellular GH mRNA are reflected by increased GH biosynthesis, suggesting that the regulation of hormone gene transcription is one cellular site for the control of hormone biosynthesis and, ultimately, hormone available for release. J. Endocr. (1986) 110, 51–57

Inhibition of L-692,429-stimulated rat growth hormone release by a weak substance P antagonist: L-756,867

1997 ◽  
Vol 152 (1) ◽  
pp. 155-158 ◽  
Author(s):  
K Cheng ◽  
L Wei ◽  
L-Y Chaung ◽  
W W-S Chan ◽  
B Butler ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Substance P ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
Gh Secretion ◽  
Substance P Antagonist ◽  
The Right ◽  
Dose Dependent

Abstract H2N,d-Arg,Pro,Lys,Pro,d-Phe,Gln,d-Trp,Phe,d-Trp,Leu, Leu,NH2 (L-756,867), a weak substance P antagonist, inhibited L-692,429-stimulated GH release from rat primary pituitary cells in a dose-dependent manner. At a concentration of 50 nm, L-756,867 shifted the dose–response curve of L-692,429-induced GH release to the right by about tenfold. It also impaired the ability of L-692,429 to potentiate the effect of growth hormone-releasing factor (GRF) on GH release. Substance P (1 μm) had no effect on basal or L-692,429-stimulated GH release. When tested in anesthetized rats, L-756,867 inhibited L-692,429- and growth hormone-releasing hexapeptide- (GHRP-6)-stimulated GH secretion in a dose-dependent manner. Complete inhibition was observed at an i.v. dose of 100 μg/kg of L-756,867. However, at the same concentration, it had no effect on GRF-induced GH secretion. d-Lys3-GHRP-6, a GHRP-6 antagonist, had no effect on GHRP-6 or L-692,429-induced GH secretion even at an i.v. dose of 2 mg/kg. These results indicate that L-692,429 and GHRP-6 stimulate GH release both in vitro and in vivo via a common receptor and signaling pathway which is different from that of substance P in spite of the fact that their effects are inhibited by a weak substance P antagonist. Journal of Endocrinology (1997) 152, 155–158

scholarly journals Expression of Chicken Thyroid-Stimulating Hormone β-Subunit Messenger Ribonucleic Acid during Embryonic and Neonatal Development*

Endocrinology ◽  
1998 ◽  
Vol 139 (2) ◽  
pp. 474-478 ◽  
Author(s):  
Charles C. Gregory ◽  
Carlton E. Dean ◽  
Tom E. Porter
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Messenger Rna ◽  
Feedback Inhibition ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Hormone Levels ◽  
Messenger Ribonucleic Acid ◽  
Thyroid Hormone Levels ◽  
D 12

Abstract The importance of thyroid hormone from embryonic through neonatal life has been documented in both avian and mammalian species. However, the regulation of thyroid hormone production during this period is not completely understood. The objective of this study was to characterize expression of chicken TSHβ messenger RNA (mRNA) compared with that of thyroid hormones and GH in embryonic and neonatal chickens. Total pituitary RNA was extracted on embryonic days (e-) 11, 13, 15, 17, and 19 and neonatal days (d-) 1, 3, 6, 9, and 12 and subjected to ribonuclease protection assays (RPA) for chicken TSHβ mRNA. TSHβ mRNA levels increased through e-19, with e-19 levels being greater than those at all other embryonic ages (P &lt; 0.05). Levels decreased markedly on d-1, then slowly increased to d-6 and stayed elevated through d-12. RIAs were performed for T4, T3, and GH at the same ages. Serum T4 levels increased slowly from less than 1.0 ng/ml on e-11 to a peak of 6.6 ng/ml on d-1 (P &lt; 0.05). After the peak on d-1, posthatch T4 levels stabilized between 3.5–4.5 ng/ml through d-12 (P &lt; 0.05). T3 concentrations were less than 0.25 ng/ml on e-11, increased dramatically between e-19 and d-1 (P &lt; 0.05), and remained high throughout the rest of the experiment, with a concentration of 3.25 ng/ml on d-6 (P &lt; 0.05). GH levels for e-11 through e-17 were below the sensitivity of the GH RIA. On e-19, the GH level was 3 ng/ml and continued to increase through d-12 to a level of 130 ng/ml. As thyroid hormone levels were preceded by maximal TSHβ mRNA levels on e-19, we next determined whether TSHβ gene expression on e-19 was under TRH and T3 regulation. E-19 anterior pituitary cells were cultured in serum-free medium with either TRH (10−8) or T3 (10−8) for 20–24 h. Treatment with T3 significantly decreased levels of TSHβ mRNA (P &lt; 0.05). However, TRH did not produce a significant increase in TSHβ mRNA, although TRH did increase TSHβ mRNA by 60%, on the average, in this study. Therefore, these results indicate that an increase in pituitary TSH production probably regulates thyroid hormone levels during late embryonic development and that negative feedback inhibition of TSH production by thyroid hormones also exists at this critical developmental stage.

Effects of hypothyroidism, tri-iodothyronine and glucocorticoids on growth hormone responses to growth hormone-releasing hormone and His-d-Trp-Ala-Trp-d-Phe-Lys-NH2

1989 ◽  
Vol 121 (1) ◽  
pp. 31-36 ◽  
Author(s):  
C. A. Edwards ◽  
C. Dieguez ◽  
M. F. Scanlon
Keyword(s):  
Growth Hormone ◽  
Thyroid Hormones ◽  
Pituitary Cells ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Monolayer Cultures ◽  
Hormone Responses

ABSTRACT The aim of this study was to investigate the role of thyroid hormones and glucocorticoids on GH secretion. Secretion of GH in response to GH-releasing hormone (GHRH) (5 μg/kg) was markedly (P < 0·001) decreased in hypothyroid rats in vivo (peak GH responses to GHRH, 635 ± 88 μg/l in euthyroid rats vs 46 ±15 μg/l in hypothyroid rats). Following treatment with tri-iodothyronine (T3; 20 μg/day s.c. daily for 2 weeks) or cortisol (100 pg/day s.c. for 2 weeks) or T3 plus cortisol, a marked (P <0·01) increase in GH responses to GHRH was observed in hypothyroid rats (peak GH responses, 326 ±29 μg/l after T3 vs 133+19 μg/l after cortisol vs 283 ± 35 μg/l after cortisol plus T3). In contrast, none of these treatments modified GH responses to GHRH in euthyroid animals. Hypothyroidism was also associated with impaired GH responses to the GH secretagogue, Hisd-Trp-Ala-Trp-d-Phe-Lys-NH2 (GHRP-6). Secretion of GH in response to GHRP-6 in vivo was reduced (P <0·01) in hypothyroid rats (peak GH responses, 508 ± 177 μg/l in euthyroid rats vs 203 ± 15 μg/l in hypothyroid rats). In-vitro studies carried out using monolayer cultures of rat anterior pituitary cells derived from euthyroid and hypothyroid rats showed a marked impairment of somatotroph responsiveness to both GHRP-6 and somatostatin in cultures derived from hypothyroid rats. In summary, our data suggest that thyroid hormones and glucocorticoids influence GH secretion by modulating somatotroph responsiveness to different GH secretagogues. Journal of Endocrinology (1989) 121, 31–36

In vitro and in vivo evidence that dopamine exerts growth hormone-releasing activity in goldfish

1993 ◽  
Vol 264 (6) ◽  
pp. E925-E932 ◽  
Author(s):  
A. O. Wong ◽  
J. P. Chang ◽  
R. E. Peter
Keyword(s):  
Growth Hormone ◽  
Body Growth ◽  
The Body ◽  
D1 Receptors ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
D1 Agonist ◽  
Plasma Gh

We have previously demonstrated that dopamine (DA) and the DA D1 agonist SKF 38393 stimulate growth hormone (GH) release from perifused pituitary fragments of the goldfish, suggesting an involvement of DA D1 receptors in GH regulation. In the present study, the role of DA on GH release and body growth of the goldfish was further investigated both in vivo and in vitro. DA consistently stimulated GH release in a dose-dependent manner from perifused goldfish pituitary fragments. The GH-releasing action of DA was seasonal, being the highest in sexually regressed fish, intermediate in recrudescent fish, and the lowest in sexually mature (prespawning) fish. Somatostatin, a known GH-release inhibitor in the goldfish, suppressed basal GH release and abolished the GH response to DA in perifused pituitary fragments as well as pituitary cells under static incubation. Intraperitoneal administration of the nonselective DA agonist apomorphine and the D1 agonist SKF 82958 increased the plasma GH levels in the goldfish. These GH responses were blocked by simultaneous treatment with the D1 antagonist Sch 23390 but not the D2 antagonist pimozide. Apomorphine administered orally also induced a similar elevation in plasma GH levels. Long-term feeding with apomorphine was found to be stimulatory to the body growth of goldfish. These results provide evidence that the neurotransmitter DA, by acting through DA D1 receptors in the pituitary, also functions as a GH-releasing factor in the goldfish.

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