Search Results
Search for other papers by J Trojan in
Google Scholar
PubMed
Search for other papers by M Theodoropoulou in
Google Scholar
PubMed
Search for other papers by KH Usadel in
Google Scholar
PubMed
Search for other papers by GK Stalla in
Google Scholar
PubMed
Search for other papers by L Schaaf in
Google Scholar
PubMed
Enhanced sialylation of thyrotropin (TSH) prolongs its metabolic clearance rate and thus increases the hormone's in vivo bioactivity. This has been shown for hypothyroid rats and for recombinant human TSH, but there are few data on the sialylation of human serum TSH. The aim of this work was to further study sialylated human serum TSH, its precursors bearing terminal galactose residues, and the role of pharmacological doses of thyrotropin-releasing hormone (TRH) on their secretion under different degrees of primary hypothyroidism. We analyzed serum TSH in patients with subclinical (n = 9) and overt primary hypothyroidism (n = 13) compared with euthyroid individuals (n = 12) and human standard pituitary TSH (IRP 80/558). Blood was drawn before and 30 min after intravenous administration of 200 micrograms TRH, and TSH was purified by immunoaffinity concentration. The content of sialylated (sialo-) TSH and isoforms bearing terminal galactose (Gal-TSH, asialo-Gal-TSH) was measured by Ricinus communis (RCA 120) affinity chromatography in combination with enzymatic cleavage of sialic acid residues. TSH immunoreactivity was measured by an automated second generation TSH immunoassay. Pituitary TSH contained 16.5 +/- 0.8% Gal-TSH. In euthyroid individuals the proportion of Gal-TSH was 14.6 +/- 1.9%, whereas TSH in patients with subclinical and overt primary hypothyroidism contained 23.9 +/- 3.5% (P < 0.05 vs euthyroid individuals) and 21.1 +/- 1.7% Gal-TSH respectively. The mean ratio of asialo-Gal TSH was 23.8 +/- 0.6% for pituitary TSH, 35.7 +/- 4.2% in euthyroid individuals, 48.0 +/- 3.3% in patients with subclinical, and 61.5 +/- 3.8% (P < 0.001 vs euthyroid individuals) in patients with overt primary hypothyroidism. For pituitary TSH the calculated proportion of sialo-TSH was 6.5 +/- 0.2%, for euthyroid individuals 20.3 +/- 2.8%, for patients with subclinical hypothyroidism 24.1 +/- 3.0%, and for patients with overt primary hypothyroidism 40.7 +/- 3.0% (P < 0.001 vs euthyroid individuals). The proportions of Gal-TSH, asialo-Gal-TSH, and sialo-TSH did not differ significantly before and after TRH administration in the individuals studied. Our data show that patients with subclinical and overt primary hypothyroidism have a markedly increased proportion of serum TSH isoforms bearing terminal galactose and sialic acid residues, which may represent a mechanism for the further stimulation of thyroid function. Pharmacological doses of TRH cause an increased quantity of TSH to be released, but do not significantly alter the proportion of sialylated or terminally galactosylated TSH isoforms.
Search for other papers by S. Harvey in
Google Scholar
PubMed
Search for other papers by S.-K. Lam in
Google Scholar
PubMed
Search for other papers by T. R. Hall in
Google Scholar
PubMed
ABSTRACT
Passive immunization of immature chickens with sheep somatostatin (SRIF) antiserum promptly increased the basal plasma GH concentration and augmented TRH-induced GH secretion. Although exogenous SRIF had no inhibitory effect on the basal GH concentration in untreated birds or birds pretreated with non-immune sheep serum, it suppressed the stimulatory effect of SRIF immunoneutralization on GH secretion. These results suggest that SRIF is physiologically involved in the control of GH secretion in birds, in which it appears to inhibit GH release tonically.
J. Endocr. (1986) 111, 91–97
Search for other papers by C. A. Ahene in
Google Scholar
PubMed
Search for other papers by R. W. Lea in
Google Scholar
PubMed
Search for other papers by S. Harvey in
Google Scholar
PubMed
ABSTRACT
Intracerebroventricular (i.c.v.) administration of GH-releasing factor (GRF) (at 1 or 10 μg) to anaesthetized immature (6- to 8-weeks-old) or adult (> 24-weeks-old) domestic fowl had no effect on basal GH concentrations in peripheral plasma, but suppressed (after 20 min) the acute GH response to exogenous (i.v.) thyrotrophin-releasing hormone (TRH) (1 μg/kg). The i.c.v. injection of GRF also reduced the content of somatostatin (SRIF) and dopamine (DA) in the hypothalamus, while increasing the concentration of the DA metabolite 3,4-dihydroxyphenyl acetic acid (DOPAC) and the DOPAC/DA ratio. The release of SRIF from hypothalamic tissue was stimulated in vitro by 100 nmol GRF/l. The inhibitory effect of i.c.v. GRF on TRH-induced GH secretion was blocked when it was simultaneously injected i.c.v. with SRIF antiserum.
These results demonstrate central effects of GRF on avian hypothalamic function and suggest an inhibitory role for this peptide in GH regulation, possibly mediated through increased SRIF secretion.
Journal of Endocrinology (1991) 128, 13–19
Search for other papers by A. E. Lamers in
Google Scholar
PubMed
Search for other papers by P. H. M. Balm in
Google Scholar
PubMed
Search for other papers by H. E. M. G. Haenen in
Google Scholar
PubMed
Search for other papers by B. G. Jenks in
Google Scholar
PubMed
Search for other papers by S. E. Wendelaar Bonga in
Google Scholar
PubMed
ABSTRACT
Using high-performance liquid chromatography (HPLC) in combination with radioimmunoassay, three forms of α-MSH (des-acetyl, mono-acetyl and di-acetyl α-MSH) were separated and identified in tilapia neurointermediate lobes and plasma, and in medium from lobes superfused in vitro. The presence of acetylated forms in lobe extracts indicated that the peptides are acetylated intracellularly. Di-acetyl α-MSH was, especially in comparison with monoacetyl α-MSH, relatively more abundant in lobe extracts than in plasma. This suggests that the three forms of α-MSH are not released according to their relative intracellular abundances. The possibility of regulation of this differential release by dopamine and TRH was investigated, using a microsuperfusion system. Dopamine was a potent inhibitor of α-MSH release, but did not modulate the relative abundance of the different forms of α-MSH released from the MSH cells. TRH was a potent stimulator of α-MSH release. It enhanced in vitro the release of di-acetyl α-MSH more than the release of mono-acetyl α-MSH. Thus tilapia may be able to modulate not only the quantitative but also the qualitative signal from the MSH cells. This might enhance the flexibility of the animals to respond to environmental challenges.
Journal of Endocrinology (1991) 129, 179–187
Search for other papers by M. Pizzi in
Google Scholar
PubMed
Search for other papers by S. Rubessa in
Google Scholar
PubMed
Search for other papers by E. Simonazzi in
Google Scholar
PubMed
Search for other papers by V. Zanagnolo in
Google Scholar
PubMed
Search for other papers by L. Falsetti in
Google Scholar
PubMed
Search for other papers by M. Memo in
Google Scholar
PubMed
Search for other papers by P. F. Spano in
Google Scholar
PubMed
ABSTRACT
Vasoactive intestinal peptide (VIP) is a prolactin-releasing hormone which is involved in the multifactorial modulation of prolactin secretion in mammals. Intravenous injection of VIP (1 μg/kg) to fertile women increased plasma prolactin levels and heart rate and reduced diastolic pressure. The same treatment to menopausal women caused similar cardiovascular effects but did not modify plasma prolactin levels. In contrast, TRH (200 μg, i.v.) induced a significant increase in plasma prolactin levels in both fertile and menopausal women. The relevance of oestrogens in affecting VIP-stimulated prolactin secretion was evaluated in vitro by measuring prolactin release from pituitary cells of control and ovariectomized rats. The sensitivity of rat mammotrophs to VIP, but not to TRH, was completely suppressed 3 or 4 weeks after ovariectomy. Furthermore, implantation of rats with a silastic capsule containing oestradiol-17β during ovariectomy, preserved the cell responsiveness to VIP. The prolactin-releasing property of VIP was also restored when pituitary cells from ovariectomized rats were cultured for 3 days in the presence of 10 nmol oestradiol-17β/l before being used for prolactin release experiments. The present study shows that the ability of prolactin-secreting cells to respond to the stimulatory action of VIP requires high levels of circulating oestrogens, both in man and rats.
Journal of Endocrinology (1992) 132, 311–316
Search for other papers by T. R. Hall in
Google Scholar
PubMed
Search for other papers by S. Harvey in
Google Scholar
PubMed
Search for other papers by A. Chadwick in
Google Scholar
PubMed
ABSTRACT
Pituitary glands and hypothalami from broiler fowl were incubated in medium containing testosterone, and prolactin and GH release were determined. Pituitary glands were also preincubated for 20 h in medium containing testosterone, and then in medium containing various secretagogues.
Testosterone inhibited the release of prolactin directly from the pituitary gland in a concentration-related manner. The hypothalamus stimulated the release of prolactin, but by a lesser amount in the presence of testosterone. When pituitary glands were preincubated with testosterone, subsequent release of prolactin was inhibited, except with the highest concentration which stimulated prolactin release. Hypothalamic extract (HE) markedly stimulated prolactin release from control pituitary glands although testosterone-primed glands were less responsive. The stimulation of prolactin release by thyrotrophin releasing hormone (TRH) and prostaglandin E2 (PGE2) was also reduced by preincubation of the pituitary glands with testosterone.
Priming with testosterone did not affect the release of GH from pituitary glands alone, but reduced the TRH-, HE- and PGE2-stimulated release of GH. These results demonstrate that testosterone directly inhibits prolactin secretion and reduces the sensitivity of pituitary lactotrophs and somatotrophs to provocative stimuli.
J. Endocr. (1984) 102, 153–159
Search for other papers by T. Noguchi in
Google Scholar
PubMed
Search for other papers by M. Kudo in
Google Scholar
PubMed
Search for other papers by T. Sugisaki in
Google Scholar
PubMed
Search for other papers by I. Satoh in
Google Scholar
PubMed
ABSTRACT
The hyt mutant mouse used in this study has a hypoplastic thyroid gland and is characterized by retarded somatic growth, very low to undetectable levels of plasma thyroxine (T4), and increased levels of plasma thyroid-stimulating hormone (TSH). This congenital hypothyroid mouse is therefore an ideal model for studying the effects of thyroid hypofunction on the adenohypophysis.
The anterior pituitary of the hyt mouse appeared less granular than that of the normal control when viewed by light microscopy, owing to a decrease in the population of somatotrophs. Many cells, in various stages of transformation into 'thyroidectomy cells', were recognized by the appearance of the characteristic granules and dilated rough endoplasmic reticulum. In some cases, the enlarged rough endoplasmic reticulum also contained spherical electron-dense secretory granules. In addition there were many cells undergoing mitosis and these were identified as thyrotrophs by their characteristic granules.
Administration of T4 during the first 40 days of life prevented the abnormal changes in the hyt anterior pituitary.
A reduction in immunoreactive thyrotrophin-releasing hormone (TRH) levels was seen in the median eminence of the hyt mouse. Treatment with T4 restored this to normal, suggesting that the reduced TRH content of the hypothalamus of the mutant mouse may be due to T4 deprivation.
J. Endocr. (1986) 109, 163–168
Search for other papers by J. O. Willoughby in
Google Scholar
PubMed
Search for other papers by H. Pederick in
Google Scholar
PubMed
Search for other papers by P. Jervois in
Google Scholar
PubMed
Search for other papers by M. Menadue in
Google Scholar
PubMed
Search for other papers by S. J. Judd in
Google Scholar
PubMed
ABSTRACT
Prolactin responses to pharmacological agents were used to characterize the defect in prolactin regulation which occurs after administration of high doses of oestrogen to rats.
Animals with chronically implanted venous cannulae were injected with 2 mg oestradiol benzoate in oil and 2–3 days later prolactin concentrations were measured after injections of saline, thyrotrophin-releasing hormone (TRH), fenfluramine, apomorphine and butaclamol. The responses were compared with those in oil-injected animals.
Hyperprolactinaemia in oestrogen-treated animals was unresponsive to apomorphine, but was even more sensitive to dopamine receptor blockade than controls. These results suggest that the lactotrophs in oestrogen-treated animals are already maximally suppressed by endogenous dopamine, though ineffectively.
Although there was an increased prolactin response to TRH in oestrogen-treated animals, there was an impaired response to fenfluramine, indicating suppressed serotonergic prolactin-releasing factor mechanisms.
Maximal endogenous dopaminergic activity and suppressed prolactin-releasing factor mechanisms are appropriate hypothalamic responses to hyperprolactinaemia. The operation of these responses in the earliest stages of the development of pituitary hyperplasia indicates that oestrogen induces a disturbance of prolactin regulation in the lactotroph, independent of hypothalamic control.
J. Endocr. (1985) 104, 447–452
Search for other papers by TAPIO RANTA in
Google Scholar
PubMed
Search for other papers by PEKKA MÄNNISTÖ in
Google Scholar
PubMed
Search for other papers by JOUKO TUOMISTO in
Google Scholar
PubMed
SUMMARY
The effects of two dopamine agonists (apomorphine and bromocriptine) and a dopamine antagonist (pimozide) on cold- or thyrotrophin releasing hormone (TRH)-induced TSH secretion were studied in normal male rats. Apomorphine given in various doses (0·5–10 mg/kg body wt) 10 min before exposure to cold significantly depressed TSH secretion. Large doses of bromocriptine (5–10 mg/kg body wt) given 1 h before exposure to cold, also blocked this response whereas a smaller dose (2·5 mg/kg body wt) given 30 min, 1, 3 or 6 h before cold exposure or repeated doses (0·1–2·5 mg/kg body wt) for 3 days did not modify cold-induced TSH secretion. Pimozide given in various doses (0·25–2·5 mg/kg body wt) 1 h before exposure to cold did not alter the cold response, but 2·5 mg/kg reversed the inhibition caused by apomorphine or bromocriptine. None of these drugs affected TRH-induced TSH secretion. These results suggest that there are no dopaminergic receptors on the pituitary thyrotrophs, but that dopamine might be an inhibitory transmitter in the brain involved in the regulation of TSH secretion in the rat.
Search for other papers by F. R. BURNET in
Google Scholar
PubMed
Search for other papers by J. B. WAKERLEY in
Google Scholar
PubMed
SUMMARY
Plasma levels of prolactin and TSH were determined by radioimmunoassay in urethane-anaesthetized lactating rats during suckling. Oxytocin release was monitored by recording intramammary pressure. Application of ten pups, 3 h after administration of urethane (1·1 g/kg, i.p.), evoked a parallel rise in prolactin and TSH concentrations which reached a maximum during the 3rd hour of suckling and then declined. Peak hormone concentrations represented a 25-fold increase in prolactin and a ten-fold increase in TSH. Suckling also elicited a pulsatile (every 5–10 min) release of 0·5–1·0 mu. oxytocin. The gradual rise in prolactin and TSH occurred between the 1st and 20th oxytocin pulses.
Intravenous injection of thyrotrophin-releasing hormone (TRH) into unsuckled, anaesthetized lactating rats resulted in a 7- to 30-fold increase in TSH concentration, whereas prolactin levels showed no substantial change.
These results indicate that suckling releases TSH as well as prolactin in the urethane-anaesthetized rat. However, the absence of prolactin release after injections of TRH makes it unlikely that both endocrine responses are regulated solely by the actions of this one releasing hormone.
