GROWTH HORMONE RELEASE FOLLOWING THYROTROPHIN-RELEASING HORMONE INJECTION INTO PATIENTS WITH ANOREXIA NERVOSA

1976 ◽  
Vol 81 (1) ◽  
pp. 1-8 ◽  
Author(s):  
K. Maeda ◽  
Y. Kato ◽  
N. Yamaguchi ◽  
K. Chihara ◽  
S. Ohgo ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Anorexia Nervosa ◽  
Luteinizing Hormone ◽  
Intravenous Injection ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Basal Plasma ◽  
Plasma Gh ◽  
Lh Rh ◽  
Plasma Prl

ABSTRACT The effect of thyrotrophin-releasing hormone (TRH) or luteinizing hormone-releasing hormone (LH-RH) on plasma levels of growth hormone (GH), prolactin (PRL), thyrotrophin (TSH), and luteinizing hormone (LH), were studied in patients with anorexia nervosa. The basal plasma GH levels were elevated in 6 of 11 patients studied. Intravenous injection of synthetic TRH (500 μg) significantly raised the plasma GH levels in 9 of 11 patients. The peak values of plasma GH after TRH ranged from 6.0 to 31.5 ng/ml. Plasma GH concentrations also increased following the administration of synthetic LH-RH (100μg) in 1 of 7 patients. The intravenous injection of saline solution caused no significant change in plasma GH in these patients. The plasma LH responses to LH-RH were significantly blunted in all patients, whereas the plasma PRL and TSH responses to TRH were almost normal in the patients examined. These results suggest that the hypothalamo-pituitary function regulating GH and LH secretion is altered in patients with anorexia nervosa.

Plasma cortisol response to thyrotrophin releasing hormone and luteinizing hormone releasing hormone in healthy kennel dogs and in dogs with pituitary-dependent hyperadrenocorticism

1982 ◽  
Vol 93 (3) ◽  
pp. 365-369 ◽  
Author(s):  
R. Stolp ◽  
R. J. M. Croughs ◽  
J. C. Meijer ◽  
A. Rijnberk
Keyword(s):  
Plasma Concentration ◽  
Luteinizing Hormone ◽  
Intravenous Injection ◽  
Plasma Cortisol ◽  
Cortisol Response ◽  
Thyrotrophin Releasing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh ◽  
Lh Releasing Hormone

The change in the plasma concentration of cortisol after the administration of thyrotrophin releasing hormone (TRH) and LH releasing hormone (LH-RH) was studied in normal dogs and in dogs with pituitary-dependent hyperadrenocorticism (PDH). The normal dogs showed a small but significant increase in the plasma concentration of cortisol 15 min after intravenous injection of TRH and LH-RH. In ten of the dogs with PDH the response to TRH was not significantly different from that in the normal dogs, but in 13 the response was significantly greater. In 15 of the dogs with PDH the response to LH-RH administration was within or below the range of responses in the normal dogs and in only one dog was the response to LH-RH greater than that in the normal dogs. These findings are discussed in relation to the pathogenesis of PDH.

VASOTOCIN RELEASE INTO THE CEREBROSPINAL FLUID OF CATS INDUCED BY LUTEINIZING HORMONE RELEASING HORMONE, THYROTROPHIN RELEASING HORMONE AND GROWTH HORMONE RELEASE-INHIBITING HORMONE

1977 ◽  
Vol 75 (1) ◽  
pp. 175-176 ◽  
Author(s):  
R. GOLDSTEIN ◽  
S. PAVEL
Keyword(s):  
Growth Hormone ◽  
Cerebrospinal Fluid ◽  
Luteinizing Hormone ◽  
Pineal Gland ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Thyrotrophin Releasing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh

Institute of Endocrinology, Bucharest, Rumania (Received 29 March 1977) The mammalian pineal gland contains (Pavel, 1965) and synthesizes (Pavel, Goldstein, Ghinea & Calb, 1977) the nonapeptide arginine-vasotocin (AVT). Since luteinizing hormone releasing hormone (LH–RH), thyrotrophin releasing hormone (TRH) and growth hormone release-inhibiting hormone (somatostatin, SRIF) have now been localized not only in the brain, but also in the pineal gland (White, Hedlund, Weber, Rippel, Johnston & Wilber, 1974; Pelletier, Le Clerc, Dube, Labrie, Puviani, Arimura & Schally, 1975), we investigated the effects of these peptides on the release of AVT into the cerebrospinal fluid (CSF) of cats. Intracarotid injections of 0·1 μg LH-RH, TRH (Hoechst, Frankfurt), SRIF (Serono, Rome) or oxytocin (Syntocinon, Sandoz Ltd, Basel) in 0·5 ml saline were given to urethane-anaesthetized male cats weighing 3–4 kg. Controls received an equal volume of saline only. The pineal glands were removed 60 min after the injections, quickly homogenized, and extracted

Stimulatory effect of thyrotrophin-releasing hormone (TRH) on the release of luteinizing hormone (LH) from rat anterior pituitary cells in vitro

1983 ◽  
Vol 61 (2) ◽  
pp. 186-189 ◽  
Author(s):  
Noboru Fujihara ◽  
Masataka Shiino
Keyword(s):  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Anterior Pituitary Cells ◽  
Lh Release ◽  
Lh Rh

The effect of thyrotrophin-releasing hormone (TRH, 10−7 M) on luteinizing hormone (LH) release from rat anterior pituitary cells was examined using organ and primary cell culture. The addition of TRH to the culture medium resulted in a slightly enhanced release of LH from the cultured pituitary tissues. However, the amount of LH release stimulated by TRH was not greater than that produced by luteinizing hormone – releasing hormone (LH–RH, 10−7 M). Actinomycin D (2 × 10−5 M) and cycloheximide (10−4 M) had an inhibitory effect on the action of TRH on LH release. The inability of TRH to elicit gonadotrophin release from the anterior pituitary glands in vivo may partly be due to physiological inhibition of its action by other hypothalamic factor(s).

HOMOLOGOUS RADIOIMMUNOASSAY FOR CANINE PROLACTIN

1977 ◽  
Vol 85 (4) ◽  
pp. 736-743 ◽  
Author(s):  
P. J. Knight ◽  
J. M. Hamilton ◽  
C. G. Scanes
Keyword(s):  
Growth Hormone ◽  
Intravenous Injection ◽  
Cross Reaction ◽  
Normal Male ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Standard Curve ◽  
Double Antibody

ABSTRACT A homologous double antibody radioimmunoassay has been developed for canine prolactin. Purified canine prolactin was iodinated by lactoperoxidase/H2O2 to an average of 101 ± 10.1 μCi/μg. Antiserum was used at a final dilution of 1:80 000 and at this concentration bound approximately 20% of the added tracer in the absence of competing unlabelled prolactin. Partial cross-reaction was observed with ovine and bovine prolactin but there was no cross-reaction with a highly purified canine growth hormone preparation. Dilutions of pregnant and lactating bitch sera were parallel to the purified canine prolactin standard curve. Mean prolactin levels in normal male and anoestrous females were 8.8 ± 0.8 and 12.6 ± 2.6 ng/ml, respectively. Thyrotrophin-releasing hormone (TRH) induced a consistent elevation in prolactin levels 15–30 min after intravenous injection.

Thyrotrophin and prolactin responses to thyrotrophin-releasing hormone in patients with Parkinson's disease

1982 ◽  
Vol 99 (3) ◽  
pp. 344-351 ◽  
Author(s):  
Abraham Martinez-Campos ◽  
Paolo Giovannini ◽  
Antonello Novelli ◽  
Daniela Cocchi ◽  
Tommaso Caraceni ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Growth Hormone ◽  
Parkinson's Disease ◽  
Chronic Treatment ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Marked Diminution ◽  
Dopaminergic Tone ◽  
Plasma Gh

Abstract. The thyrotrophin (TSH) and prolactin (Prl)-releasing effects of TSH-releasing hormone (TRH) were investigated in 20 subjects with Parkinson's disease (PD), unmedicated, on chronic treatment with a combination levodopa-benserazide (Madopar) or levodopa-carbidopa (Sinemet) or withdrawn from therapy. Administration of TRH (200 μg iv) induced in unmedicated patients TSH and Prl responses significantly lower than those of sex-and age-matched controls. In patients on Madopar therapy the TSH and Prl responses to TRH were greater than in unmedicated patients and comparable to those of controls, while in patients on Sinemet therapy the pituitary responses were undistinguishable from those of unmedicated subjects. Withdrawal of Madopar therapy resulted in a marked diminution of the TSH response but did not affect the Prl response to TRH. Withdrawal of Sinemet therapy did not alter the TSH and Prl responses to TRH. Concomitant evaluation of growth hormone (GH) levels, in none of the subjects evidenced non-specific changes in plasma GH following TRH. Since TSH and Prl responses to TRH are inhibited by an enhancement of the dopaminergic tone, it would appear that the latter is preserved in the tuberoinfundibular system of unmedicated subjects and subjects on chronic Sinemet therapy, but is defective in subjects on chronic Madopar therapy.

THE DYNAMICS OF GROWTH HORMONE AND PROLACTIN SECRETION IN ACROMEGALIC PATIENTS WITH "MIXED" PITUITARY TUMOURS

1979 ◽  
Vol 90 (2) ◽  
pp. 198-210 ◽  
Author(s):  
Steven W. J. Lamberts ◽  
Jan G. M. Klijn ◽  
Giok H. Kwa ◽  
Jan C. Birkenhäger
Keyword(s):  
Growth Hormone ◽  
Pituitary Adenomas ◽  
Suppressive Effect ◽  
Oral Glucose ◽  
Delayed Response ◽  
Thyrotrophin Releasing Hormone ◽  
Lowering Effect ◽  
Close Relationship ◽  
Plasma Gh ◽  
Plasma Prl

ABSTRACT The dynamics of growth hormone (GH) and prolactin (PRL) secretion in response to thyrotrophin-releasing hormone (TRH) and bromocriptine were evaluated in 15 untreated and 1 previously unsuccessfully treated patients with acromegaly. In 7 of these patients elevated basal PRL levels were found. In 4 of the 7 hyperprolactinaemic patients plasma PRL concentrations followed closely the pattern of GH secretion in response to TRH (400 μg). The maximal paradoxical increment of GH in response to TRH was paralleled by a delayed PRL response, while a close relationship was observed between the suppression of the elevated GH and PRL levels in these patients after one single dose of 2.5 mg bromocriptine. In one of these patients parallel escapes of plasma GH and PRL during bromocriptine treatment were seen. In addition, a significant higher sensitivity to the GH-lowering effect of 2.5 mg bromocriptine was noted from 2 up to 8 h in these 4 patients with presumably "mixed" GH/PRL secreting pituitary adenomas, compared with the response in 9 untreated acromegalic patients with normal basal PRL levels. In the 3 acromegalic patients with slightly elevated PRL levels, no or a normal increase of PRL levels in response to TRH was observed, while the suppressive effect of bromocriptine on plasma GH concentrations was not different from that seen in the acromegalic patients with normal PRL levels. However, as a group the 7 patients with hyperprolactinaemia showed a significantly higher GH-lowering effect to 2.5 mg bromocriptine than the 9 normoprolactinaemic acromegalic patients. A close relationship between the magnitude of the increment of GH in response to TRH and the decrease of plasma GH after 2.5 mg bromocriptine was present in the whole group of 16 acromegalics (P < 0.01). No such correlation was shown in the type of response of plasma GH to an oral glucose load or the coefficient of variation of basal plasma GH levels on 5 different days. It is concluded that in the population of acromegalic patients with elevated plasma PRL levels a sub-population of patients is present with "mixed" pituitary adenomas which secrete GH and PRL in a parallel manner. The characteristics of the secretion of both hormones, in these patients can be recognized as a parallel, delayed response of both hormones to TRH and an increased sensitivity to the suppressive effect of bromocriptine.

Hypothalamic hormones that release growth hormone stimulate hepatic 5′-monodeiodination activity in the chick embryo

1988 ◽  
Vol 118 (2) ◽  
pp. 233-236 ◽  
Author(s):  
E. R. Kühn ◽  
A. Vanderpooten ◽  
L. M. Huybrechts ◽  
E. Decuypere ◽  
V. Darras ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Plasma Concentration ◽  
Chick Embryo ◽  
Chick Embryos ◽  
Thyrotrophin Releasing Hormone ◽  
Growth Hormone Releasing Factor ◽  
Releasing Hormone ◽  
Pancreatic Growth ◽  
Hypothalamic Hormones ◽  
Plasma Gh

ABSTRACT Plasma GH, tri-iodothyronine (T3), thyroxine (T4) and liver 5′-monodeiodination (5′-D) activity were measured in 18-day-old chick embryos injected with thyrotrophin-releasing hormone (TRH) and human pancreatic growth hormone releasing factor (hpGRF). Injections of 0·1 and 1 μg TRH and 1·5 μg hpGRF increased the concentration of plasma GH while injection of 15 μg hpGRF had no effect. Concentrations of plasma T3 were raised after injection of TRH or hpGRF. Injections of TRH but not of hpGRF raised the concentration of plasma T4. The increases in concentration of plasma T3 after injection of TRH or hpGRF were parallelled by increases in liver 5′-D activity. An injection of 0·25 μg T4 significantly raised the concentration of T4 in plasma but had no effect on plasma T3 or liver 5′-D activity. It is concluded that the release of chicken GH by TRH or hpGRF is responsible for the observed increases in plasma concentration of T3 and liver 5′-D activity. J. Endocr. (1988) 118, 233–236

PITUITARY HORMONE RESPONSES TO HYPOTHALAMIC RELEASING HORMONES IN ACROMEGALY

1976 ◽  
Vol 83 (4) ◽  
pp. 673-683 ◽  
Author(s):  
L. Cantalamessa ◽  
E. Reschini ◽  
A. Catania ◽  
G. Giustina
Keyword(s):  
Clinical Signs ◽  
Pituitary Function ◽  
Pituitary Hormone ◽  
Repeated Testing ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Prolactin Response ◽  
Plasma Gh ◽  
Lh Rh ◽  
Pituitary Irradiation

ABSTRACT The pituitary reserve of GH, prolactin, TSH, LH, and FSH has been studied in a group of 13 acromegalic patients with the aim of evaluating the pituitary function and the activity of the disease. Plasma GH, TSH and prolactin were determined after thyrotrophin releasing hormone (TRH) administration, plasma gonadotrophins and GH after luteinizing hormone releasing hormone (LH-RH) administration. The plasma TSH response to TRH was generally blunted in the patients treated with pituitary irradiation; however, none of the patients with diminished TSH reserve had signs of hypothyroidism. Six acromegalics showed prolactin basal levels higher than controls; none had galactorrhoea; 4 of them complained of impairment of the gonadal function. The prolactin response to TRH was variable and not related to prolactin basal levels. A subnormal LH reserve after LH-RH stimulation was observed in 5 out of 10 patients; 4 of them had also clinical signs of hypogonadism. A normal FSH response to LH-RH was present in all patients. A non-specific GH response to TRH and/or LH-RH was obtained in about half of the acromegalics studied. The GH responsiveness to TRH and/or LH-RH was not related to the activity of the disease or to a specific derangement of the hypothalamo-pituitary function. A concordant response was observed only between GH and prolactin response to TRH; the highest prolactin responses to TRH were obtained in the GH responsive patients. Each patient showed a constant GH pattern of response on repeated testing. Even after pituitary irradiation the pattern of GH response was unchanged in spite of lowered GH plasma levels.

EFFECTS OF LUTEINIZING HORMONE RELEASING HORMONE ON PLASMA FOLLICLE-STIMULATING HORMONE AND LUTEINIZING HORMONE LEVELS IN THE FERRET

1977 ◽  
Vol 73 (1) ◽  
pp. 37-52 ◽  
Author(s):  
B. T. DONOVAN ◽  
M. B. TER HAAR
Keyword(s):  
Luteinizing Hormone ◽  
Intravenous Injection ◽  
Follicle Stimulating Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Hormone Levels ◽  
Oestradiol Treatment ◽  
Gonadotrophin Secretion ◽  
Lh Rh ◽  
Lh Secretion

SUMMARY Heterologous radioimmunoassays for FSH and LH were employed to examine the effect of synthetic LH-RH upon gonadotrophin secretion in the ferret. Intravenous injection of 4 μg LH-RH induced a surge of FSH and of LH secretion in male and in female animals. In intact and in castrated males, the rise of LH was much more marked than that of FSH. The gonadotrophin response to LH-RH was greater in anoestrous than in oestrous females; FSH secretion was not enhanced during oestrus. Ovariectomized females behaved as anoestrous females with respect to LH secretion, while FSH secretion remained unchanged. Treatment of ovariectomized females with progesterone did not alter the pattern of response to LH-RH, but oestradiol treatment depressed the reaction to match that seen in oestrous females. Repetitive injections of LH-RH induced repetitive surges of FSH and LH in anoestrous females, but only of LH during oestrus: slow i.v. infusion of LH-RH induced a sustained elevation of plasma LH levels both in oestrous and in anoestrous females; again FSH levels rose only in anoestrous females. Injection of synthetic TRH did not alter gonadotrophin secretion in corresponding groups of male or female ferrets.

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