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PubMed1987

Chronic food restriction and the circadian rhythms of pituitary-adrenal hormones, growth hormone and thyroid-stimulating hormone.

Adult male Sprague-Dawley rats were subjected to food restriction so that they ate 65% of food ingested by control rats. While control rats had free access to food over the 24-hour period, food-restricted rats were provided with food daily at 10 a.m. The experimental period lasted for 34 days. On day 35, rats from both experimental groups were killed at 08.00, 11.00, 14.00, 24.00 and 02.00 h. Food restriction modified the circadian rhythms of ACTH and corticosterone. In addition, total circulating corticosterone throughout the day was higher in food-restricted than in control rats. In contrast, food restriction resulted in depressed secretion of thyroid-stimulating hormone and growth hormone. The results indicate that time of food availability entrained circadian corticosterone rhythm but not thyroid-stimulating hormone and growth hormone rhythms.

Adrenal Glands↗
PubMed1985

Thyroid-stimulating hormone, prolactin, and growth hormone response to thyrotropin-releasing hormone in treated children with congenital hypothyroidism.

The purpose of the present study was to assess thyroid-stimulating hormone (TSH), prolactin, and growth hormone responses to TRH stimulation in 12 congenitally hypothyroid children adequately treated with L-thyroxine from the first weeks of life. Although clinically euthyroid, six of these children were found to have abnormally high basal serum TSH concentrations despite clinical euthyroidism. Serum triiodothyroxine and L-thyroxine concentrations were normal and did not differ whether the children had elevated or normal basal serum TSH. All six of the children with high basal TSH had an exaggerated TSH response to TRH and 4 of them also had an augmented prolactin response to TRH. The children with normal basal TSH concentrations had normal TSH and prolactin responses to TRH. An abnormal ("paradoxical") elevation of growth hormone concentration in response to TRH was found in four of seven children in a separate group of patients who had prolonged, untreated primary hypothyroidism, but such responses were not found in any of the adequately treated children. These findings suggest the following conclusions: 1) the phenomenon of high serum concentrations of TSH in conjunction with normal L-thyroxine and triiodothyronine levels (and clinical euthyroidism), is prevalent in congenital hypothyroid patients. 2) These patients have an exaggerated response of their pituitary thyrotroph and lactotroph cells to TRH, presumably caused by selective and relative resistance of these cells to the inhibitory effects of thyroid hormones. 3) Congenital hypothyroidism is not associated with abnormal somatotroph cell responses to TRH.

Adolescent↗
PubMed1977

Release of luteinizing hormone releasing hormone and thyrotropin releasing hormone from a synaptosome-enriched fraction of hypothalamic homogenates.

A mitochondrial fraction prepared from homogenates of rat hypothalamic tissue was found by means of electron microscopy to be enriched with synaptosomes. The release of luteinizing hormone releasing hormone (LHRH) and thyrotropin releasing hormone (TRH) from this preparation was investigated. After incubation, the synaptosomes were re-isolated by ultrafiltration; and the concentration of LHRH and TRH in the ultrafiltrate was determined by radioimmunoassay. When the synaptosome-enriched preparation was incubated in 0.32M sucrose at 1 or 30 C, less than 10% of the total LHRH and TRH was recovered in the ultrafiltrate. The two hormones were released by depolarizing concentrations (60 mM) of K+ in a Ca++-dependent manner, and the stimulatory effect of K+ was essentially complete within 2 min. In the presence of 2 mM Ca++, the release of LHRH and TRH increased with increasing K+ concentrations in the range 30-120 mM. Prostaglandin E2 (PGE2), PGF2 alpha, and PGF2 beta had little if any effect on LHRH or TRH release. When the synaptosome-enriched fraction was incubated in Hanks' balanced salt solution, the release of LHRH and TRH was about 10 times greater than that seen in 0.32M sucrose. It is concluded that a synaptosome-enriched fraction from the hypothalamus contains readily releasable pools of LHRH and TRH which are mobilized rapidly by depolarizing concentrations of K+ in a Ca++-dependent manner.

Animals↗
PubMed2001

Diagnostic value of pituitary MRI in differentiation of children with normal growth hormone secretion, isolated growth hormone deficiency and multiple pituitary hormone deficiency.

Pituitary height, volume and morphology were investigated by MRI in patients aged 3.5-24.9 years with growth hormone deficiency (GHD) in relation to birth history and hormonal findings. Three groups with comparable age, sex and pubertal stage were studied: group I (n=42)--patients with isolated growth hormone deficiency (IGHD); group II (n=22)-- patients with multiple pituitary hormone deficiency (MPHD); and group III (n=30)--healthy controls. Pituitary height and volume differed significantly between the three groups, with the smallest in group II and largest in group III (p <0.001 for both). Both variables correlated significantly with peak GH value in the patient groups (p <0.001). The specificity of pituitary dysmorphology in the determination of GHD was 100% and its sensitivity in differentiation of IGHD and MPHD was 95%. Ectopic neurohypophysis was present in 75% of breech births and 27% of head-presenting patients (p <0.01). This study emphasizes the differential diagnostic value of pituitary MRI and its contribution to the understanding of the pathogenesis and prognosis in GHD.

Adolescent↗
PubMed1984

Changes in plasma thyrotrophin-releasing hormone, thyrotrophin, prolactin and thyroid hormone levels after intravenous, intranasal or rectal administration of synthetic thyrotrophin-releasing hormone in man.

Changes in plasma thyrotrophin-releasing hormone (TRH), thyrotrophin (TSH), prolactin and thyroid hormone levels after iv, intranasal, or rectal administration of synthetic TRH were studied in man. The plasma TRH concentration increased with all three routes, but remained at higher levels for a longer time after intranasal or rectal administration, in contrast to the rapid decrease after iv administration. Plasma TSH, prolactin and thyroid hormone levels increased significantly after intranasal or rectal administration and also remained elevated for a longer period than iv administration. These findings suggest that TRH administered intranasally or rectally enters the blood stream and stimulates TSH, prolactin and thyroid hormone release in man.

Administration, Intranasal↗
PubMed1989

The effects of treatment combining an agonist of gonadotropin-releasing hormone with growth hormone in pubertal patients with isolated growth hormone deficiency.

The final height of patients treated with growth hormone for isolated growth hormone deficiency has, up to now, been subnormal, with a mean below -2 SD in the series reported, an insufficient height at the onset of puberty and a more or less accelerated bone maturation during puberty being two important factors of the poor results. A long-acting analogue of gonadoliberin, Trp6-GnRH, has been given to GH-treated patients with isolated growth hormone deficiency at the time they reached pubertal stage 2, in combination with unchanged doses of GH, for one year in 11 and for two years in 7 of them. It resulted in an increase in the height age/bone age ratio and a reduction of the height insufficiency for bone age. The increase was slight but significant after one year, and fair after two years, in spite of reduced annual growth rate. Post-analogue follow-up in 5 patients with continued GH treatment showed a good development of growth and of puberty. It is concluded that combination of the long-acting Trp6-GnRH analogue and GH for 1-2 years in patients with isolated growth hormone deficiency whose puberty starts with a very insufficient height may be an appropriate way to improve their growth parameters. Studies with increased doses of GH or increased frequency of injections could help to optimize the results. Several years of follow-up are needed for demonstrating the results on final height.

Adolescent↗
PubMed1977

Oestrogen-induced changes in the secretion of luteinizing hormone caused by continuous infusions of luteinizing hormone releasing hormone in the long-term ovariectomized rat.

Oestrogen-induced changes in luteinizing hormone secretion, caused by continuous infusions of luteinizing hormone releasing hormone (LH-RH), appear to depend on the duration of exposure of the pituitary gland to the releasing hormone. The initial oestrogen-induced depression of the potential response of the pituitary gland to LH-RH, which always seems to occur, does not necessarily turn into an enhancement of this potential response. It is suggested that this may be due to the fact that the response of the pituitary gland to LH-RH infusions is a continuously changing parameter influenced by oestrogen.

Animals↗
PubMed1990

Alterations of serum concentrations of thyroid hormones and sex hormone-binding globulin, nuclear binding of tri-iodothyronine and thyroid hormone-stimulated cellular uptake of oxygen and glucose in mononuclear blood cells from patients with non-thyroidal illness.

Nuclear tri-iodothyronine (T3) binding and thyroid hormone-stimulated oxygen consumption and glucose uptake were examined in mononuclear blood cells from patients with non-thyroidal illness (NTI) in which serum T3 was significantly (P less than 0.05) depressed (0.62 +/- 0.12 (S.D.) nmol/l) compared with healthy control subjects (1.45 +/- 0.30 nmol/l). Neither serum TSH nor sex hormone-binding globulin differed from that of the control group. Nuclear T3 binding capacity was increased (P less than 0.05) in patients with NTI (10.1 +/- 3.0 fmol/100 micrograms DNA) compared with controls (2.5 +/- 0.9 fmol/100 micrograms DNA). Unstimulated glucose uptake was increased in cells from patients with NTI (2.03 +/- 0.49 mmol/l per mg DNA per h, P less than 0.01) compared with controls (1.13 +/- 0.20 mmol/l per mg DNA per h). Thyroxine-stimulated glucose uptake (stimulated glucose uptake--unstimulated glucose uptake) was increased in cells from patients with NTI (2.06 +/- 1.67 mmol/l per mg DNA per h, P less than 0.01) compared with controls (0.26 +/- 0.12 mmol/l per mg DNA per h), and T3-stimulated glucose uptake was also increased in cells from patients with NTI (1.34 +/- 0.81 mmol/l per mg DNA per h, P less than 0.05) compared with controls (0.24 +/- 0.10 mmol/l per mg DNA per h). In contrast, neither unstimulated nor thyroid hormone-stimulated oxygen consumption differed. We conclude that both increased nuclear T3 binding and increased thyroid hormone-induced glucose uptake may represent counter-regulatory mechanisms which tend to maintain intracellular homeostasis.

Adult↗
PubMedDate not supplied

Different effects of growth hormone-releasing hormone (GRH) and somatostatin on growth hormone and stable metabolite of prostaglandin E2, 13, 14-dihydro-15-keto-prostaglandin E2 (PGE2-M) in normal subjects.

Twenty four healthy subjects were placed in two treatment groups: 1. The first group consisted of twelve subjects in whom growth releasing hormone (GRH) (1 microgram/kg.BW) resulted in a marked and sustained elevation of serum growth hormone (GH) and a slight and delayed increase in plasma prostaglandin E2-M. In the second group, consisting also of twelve subjects, somatostatin infusion (500 micrograms/250 ml) was initiated and maintained for 60 min. Serum GH significantly decreased at 30 and 60 min during infusion and 15 min thereafter. We did not observe any changes in plasma prostaglandin E2-M during or after somatostatin infusion. The results obtained confirm previous in vitro studies and suggest a possible link between growth releasing hormone and prostaglandin E2 in their action on growth hormone secretion. It seems that somatostatin does not play a role in the control of prostaglandin E2 release.

Adult↗
PubMed1988

Morphological study of the rat pituitary follicle stimulating hormone cells after alternate day treatment with luteinizing hormone-releasing hormone (LHRH).

The action of the luteinizing hormone-releasing hormone (LHRH) on the hypophyseal gonadotrophins has either an activatory or inhibitory effect depending on the doses administered or on the treatment followed. Both factors can induce a different response in the two hormones. In this work, the effect after the administration of 8 doses (40 micrograms/day) of LHRH at intervals of 48 hours, on the serum levels of follicle stimulating hormone (FSH), as well as the numerical density, distribution, intensity of staining and morphometrical parameters of the cells which react against the anti-FSH serum, are assessed. It has been found that with the treatment an increase of FSH serum levels, without modification in the number of immunoreactive cells, but a clear increase in the lightly stained cells, is produced. The distribution of the reactive cells, uniform in normal animals, shows a large numerical density in the dorsal and posterior hypophyseal areas in the treated animals. No change was observed in the nuclear and cellular areas between the different groups.

Animals↗
PubMed1984

Stimulation of growth hormone secretion by human pancreatic growth-hormone-releasing factor and thyrotrophin-releasing hormone in anaesthetized chickens.

Sodium pentobarbitone anaesthesia depressed the concentration of growth hormone (GH) in the plasma of young (6 weeks of age) and old (22-30 weeks of age) domestic fowl. In both cases the concentration was reduced (P less than 0.05) within 10 min and had declined (P less than 0.001) to stable low levels (less than 5 ng/ml) within 50 min. The intravenous administration of synthetic human pancreatic growth-hormone-releasing factor (hpGRF) (10 micrograms/kg) (2 X 10(-9) mol/kg) increased (P less than 0.01) the GH concentration in both the young and old birds. This effect was observed irrespective of whether the birds were conscious or anaesthetized. The magnitude of the response in conscious young birds (164 ng/ml) was, however, greater (P less than 0.01) than that in anaesthetized chicks (64 ng/ml). The response in anaesthetized adult fowl (18.8 ng/ml) was also less (P less than 0.05) than that in their conscious counterparts (42.8 ng/ml). The GH response in conscious and anaesthetized 6-week-old birds to hpGRF was greater (P less than 0.01) than that in the corresponding adult birds. Thyrotrophin-releasing hormone (TRH) (10 micrograms/kg (2.8 X 10(-8) mol/kg); iv) also provoked (P less than 0.01) GH secretion in conscious and anaesthetized young birds and in anaesthetized (but not conscious) adults. Anaesthesia blunted (P less than 0.01) the GH response to TRH in the immature cockerels, although the response was greater (P less than 0.05) than that in anesthetized adults.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1985

Growth hormone, thyrotropin and prolactin responses to simultaneous administration of human growth hormone-releasing factor and thyrotropin releasing hormone in the bovine.

The effects of intravenous injection of synthetic human pancreatic growth hormone-releasing factor-44-NH2 (hpGRF-44) and synthetic thyrotropin releasing hormone (TRH), or hpGRF-44 in combination with TRH on growth hormone (GH), thyrotropin (TSH), and prolactin (PRL) release in dairy female calves (6- and 12-month-old) were studied. When 0.25 microgram of hpGRF-44 per kg of body weight (bw) was injected in combination with TRH (1.0 microgram per kg of bw), the mean plasma GH concentration of the 12-month-old calves rose to a maximum level of 191.5 ng/ml (P less than 0.001) at 15 min from the value of 6.8 ng/ml before injection at 0 min. The maximum level was 3.1 and 6.1 times as high as the peak values obtained after injection of hpGRF-44 (0.25 microgram per kg of bw) and TRH (1.0 microgram per kg of bw), respectively (P less than 0.001). The area under the GH response curve for the 12-month-old calves for 3 hr after injection of hpGRF-44 in combination with TRH was 2.5 times as large as the sum of the areas obtained by hpGRF-44 and TRH injections. In contrast, the mean plasma GH level was unchanged in saline injected calves. The magnitudes of the first and the second plasma GH responses in the 6-month-old calves to two consecutive injections of hpGRF-44 in combination with TRH at a 3-hr interval were very similar. The peak values of plasma GH in the calves after hpGRF-44 injection were 2-4 times as high as those after TRH injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Stimulation of growth hormone release in dwarf and normal chickens by thyrotrophin releasing hormone (TRH) or human pancreatic growth hormone releasing factor (hpGRF).

The effect of thyrotrophin releasing hormone (TRH) or human pancreatic growth hormone releasing factor (hpGRF) on growth hormone (GH) release was studied in both dwarf and normal Rhode Island Red chickens with a similar genotype except for a sex-linked dw gene. Both TRH (10 micrograms/kg) and hpGRF (20 micrograms/kg) injections stimulated plasma GH release within 15 min in young and adult chickens. The increase in GH release was higher in young cockerels than that in adult chickens. The age-related decline in the response to TRH stimulation was observed in both strains, while hpGRF was a still potent GH-releaser in adult chickens. The maximal and long acting response was observed in young dwarf chickens, suggesting differences in GH pools releasable by TRH and GRF in the anterior pituitary gland. The pituitary gland was stimulated directly by perifusion with hpGRF (1 microgram/ml and 10 micrograms/ml) or TRH (1 microgram/ml). Repeated perifusion of GRF at 40 min intervals blunted further increase in GH release, but successive perifusion with TRH stimulated GH release. The results suggest the possibility that desensitization to the effects of hpGRF occurs in vitro and that the extent of response depends on the number of receptors for hpGRF or TRH and/or the amount of GH stored in the pituitary gland.

Age Factors↗
PubMed1978

The effect of varying prolactin levels on pituitary luteinizing hormone and follicle-stimulating hormone response to gonadotropin-releasing hormone.

Seventy-one women with menstrual irregularities were investigated by measurement of basal plasma estradiol, prolactin, and gonadotropin levels. They were each given an intravenous injection of 100 microgram of gonadotropin-releasing hormone (GnRH), and both luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured for two hours. The women were divided into three groups on the basis of the prolactin levels: "normal," "mild elevation," and "severe elevation." For each prolactin group there was no difference in age or estradiol or basal LH and FSH levels. The pituitary response to the GnRH injection was also similar for the three groups. These data suggest that elevated prolactin levels do not interfere with pituitary gonadotropin cell function.

Estradiol↗
PubMed1985

Growth hormone secretion in anaesthetized fowl. 2. Influence of heterologous stimuli in birds refractory to human pancreatic growth hormone-releasing (hpGRF) or thyrotrophin releasing hormone (TRH).

In anaesthetized young (6 weeks old) and adult (22-30 weeks old) domestic fowl, the administration of thyrotrophin releasing hormone (TRH; 1.0 micrograms/kg in young birds; 10.0 micrograms/kg in adults) or human pancreatic growth hormone-releasing factor (hpGRF(1-44)NH2; 10.0 micrograms/kg in both cases) markedly increased the growth hormone (GH) concentration in plasma samples collected 10 min later. In birds injected with TRH, this stimulation of GH secretion attenuated the GH response to a second TRH challenge (given 15 or 60 min after the first in adult or young birds, respectively); similarly, hpGRF pretreatment blunted the GH response to a further hpGRF injection. However, the administration of hpGRF to both immature and adult birds made refractory to TRH challenge was followed by increased GH secretion and vice versa. Moreover, the GH secretory response to hpGRF in birds pretreated with TRH was greater (1.99-fold in young birds, 1.52-fold in adults) than the increase in plasma GH concentration following hpGRF administration in untreated birds. Similarly, prior exposure to hpGRF also increased the GH response to TRH stimulation (by 2.24-fold in the young, 3.56-fold in the adults). These results demonstrate that TRH not only overcomes GH refractoriness to hpGRF and vice versa, but the GH response to heterologous provocative stimuli is potentiated in birds refractory to TRH or hp GRF challenge.

Anesthesia↗
PubMed1989

Possible participation of calcium in growth hormone release and in thyrotropin-releasing hormone and human pancreatic growth hormone-releasing factor synergy in a primary culture of chicken pituitary cells.

We previously reported that thyrotropin-releasing hormone (TRH) and human pancreatic growth hormone-releasing factor (hpGRF) exert synergistic (greater than additive) effects on growth hormone (GH) release from chicken pituitary cells in primary culture. In the present studies the possible participation of calcium in GH release and in TRH and hpGRF synergy was investigated. Following dispersion with collagenase, cells were cultured for 48 hr prior to exposure (2 hr) to test agents. Cultured cells were exposed to a range of calcium concentrations (0, 0.02, 0.2, and 2.0 mM) in the presence and absence of secretagogues. These results demonstrated that basal GH release was not altered by the concentration of calcium in the medium: however, secretagogue-induced GH release required calcium. Thus, TRH, hpGRF, 8 Br-cAMP, or forskolin stimulated GH release in the absence of calcium. Furthermore, synergistic GH release evoked by TRH and hpGRF, 8 Br-cAMP, or forskolin was observed only at the highest calcium concentration (2.0 mM). In other studies, ionomycin (10(-5) M), a calcium ionophore, stimulated GH release to a value about 125% over the basal (absence of test agent) value. Ionomycin-induced GH release was not affected by TRH (5.0 ng/ml); the combined effects of ionomycin (10(-7)-10(-5) M) and hpGRF (5.0 ng/ml) on GH release were less than additive. However, ionomycin (10(-5) M) further increased GH release over that resulting from the synergistic action of TRH and hpGRF (5.0 ng/ml each). Verapamil (a calcium channel blocker) did not affect GH release induced by either TRH or hpGRF (5.0 ng/ml each). However, this agent did inhibit synergistic GH release evoked by TRH and hpGRF, 8 Br-cAMP, forskolin, or isobutylmethylxanthine. These results suggest that calcium participates in secretagogue-induced GH release from chicken somatotrophs in vitro.

Animals↗
PubMed1989

Acute inhibition of somatotroph response to human growth hormone-releasing hormone 1-44 occurs following three hours but not one hour of growth hormone infusion.

Our previous studies have demonstrated that a short-term (three hour) infusion of methionyl human growth hormone (met-hGH, 2 micrograms/kg/h) is associated with a rise in serum concentrations of free fatty acids and glycerol, and a blunting of somatotroph response to human growth hormone releasing hormone 1-44 (GRH) in normal volunteers. To gain more information on the time course of this blunting, and to determine whether it could be temporally dissociated from the GH-induced rise in serum concentrations of lipolytic products, the response to GRH (0.3 micrograms/kg) was measured in five normal adult volunteers from hours 1.0 to 3.5 of a 3.5-hour infusion of saline or met-hGH 2 micrograms/kg/h. Somatotroph response to the same dose of GRH from hours 3.0 to 5.5 of a longer (5.5-hour) infusion of saline or met-hGH (2 micrograms/kg/h) in five other volunteers was used for comparison. There was a significant blunting of somatotroph response following three hours, but not one hour of met-hGH infusion. The longer infusion was associated with a significant rise in serum concentrations of free fatty acids, and the shorter met-hGH infusion was too brief to provoke such a rise. Neither met-hGH infusion was associated with a significant rise in serum concentrations of glycerol, insulin, glucose, or insulin-like growth factors (IGF). This study provides further evidence that there is an association between circulating FFA and somatotroph function and suggests that FFA may act as messengers, which provide information to central systems regarding the energy balance of the organism.

Adult↗
PubMed1993

Effect of regularity of exposure to chronic immobilization stress on the circadian pattern of pituitary adrenal hormones, growth hormone, and thyroid stimulating hormone in the adult male rat.

Circadian variation of serum levels of adrenocorticotropin hormone (ACTH), corticosterone, growth hormone (GH), and thyroid-stimulating hormone (TSH) were studied in three groups of adult male rats exposed to chronic intermittent immobilization stress (IMO) for 2 hr daily under different schedules. IMO resulted in reduced food intake, body weight loss, and increased adrenal weight. ACTH levels were not affected but corticosterone levels were increased in all IMO rats as compared to control ones during the diurnal phase of the circadian cycle. IMO decreased serum GH and TSH levels but the circadian pattern of secretion was influenced in a complex way depending on the specific pattern of daily exposure to IMO. Differences observed between the IMO groups were not caused by differences in food intake because its circadian rhythm was very similar in all IMO groups. These results suggest that regularity of exposure to immobilization alters in a complex fashion circadian GH and TSH rhythms.

Adrenal Cortex Hormones↗