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Showing papers on "Prolactin published in 1989"


Journal ArticleDOI
TL;DR: A novel neuropeptide which stimulates adenylate cyclase in rat anterior pituitary cell cultures was isolated from ovine hypothalamic tissues and increased release of growth hormone, prolactin, corticotropin and luteinizing hormone from superfused rat pituitaries at as small a dose as 10(-10)M) or 10(-9)M (LH).

1,815 citations


Journal ArticleDOI
TL;DR: There is a high incidence of anterior pituitary hormone deficiencies in patients treated surgically forpituitary tumours and the incidence increases after external radiotherapy and endocrine testing is recommended on an annual basis.
Abstract: The development of anterior pituitary hormone deficiencies has been studied in a group of 165 patients who underwent external radiotherapy for tumours of the pituitary or closely related anatomical sites, and who have been observed for up to 10 years. One hundred and forty had undergone pituitary surgery before radiotherapy. All patients received external radiotherapy by a three-field technique, giving 3750-4250 cGy in 15 or 16 fractions over 20-22 days. A combined test of anterior pituitary function using insulin hypoglycaemia or glucagon stimulation in conjunction with thyrotrophin and gonadotrophin releasing hormone tests and basal estimations of prolactin, thyroid hormones and testosterone or oestradiol was performed before radiotherapy. This was repeated six and 12 months later and subsequently annually. Before radiotherapy, 18 per cent of patients had normal growth hormone secretion, 21 per cent had normal gonadotrophin secretion, 57 per cent had normal corticotrophin reserve and 80 per cent had normal thyrotrophin secretion. Life table analysis demonstrated increasing incidences of all anterior pituitary hormone deficiencies with time: by five years all patients were growth hormone deficient, 91 per cent were gonadotrophin deficient, 77 per cent were corticotrophin deficient and 42 per cent were thyrotrophin deficient. At eight years, respective incidences of deficiencies were 100, 96, 84 and 49 per cent. Radiation-induced hyperprolactinaemia was seen in 73 patients; mean serum prolactin concentration rose from 227 +/- 11 mU/l to a peak of 369 +/- 60 mU/l at two years and subsequently declined towards the basal value. The primary diagnosis, patient age, sex, irradiated tissue volume and previous surgery were examined as variables that might influence the rate of development of anterior pituitary hormone deficiencies, but none of these factors had a significant effect. The radiation induced hyperprolactinaemia was however more marked in female patients. Although anterior pituitary hormone deficiencies most commonly developed in the order growth hormone, gonadotrophin, corticotrophin, thyrotrophin (61 per cent of patients), other sequences were evident. Most notably corticotrophin deficiency occurred before gonadotrophin deficiency. There is a high incidence of anterior pituitary hormone deficiencies in patients treated surgically for pituitary tumours and the incidence increases after external radiotherapy. Deficiencies may occur in an unpredictable sequence and endocrine testing is recommended on an annual basis.

419 citations


Journal ArticleDOI
TL;DR: It is quite possible that the increased immune response in females allows them to compensate for the increased physiological stress which accompanies reproduction, and the final outcome would thus be the assurance of reproductive success of the species.

334 citations


Journal ArticleDOI
TL;DR: Interleukin-6 (IL-6), a cytokine produced by inflammatory reactions, was found to stimulate PRL, GH and LH release from anterior pituitary cells at concentrations similar to those which affected lymphocyte mitogenesis to demonstrate a new biological activity for IL-6 and provide evidence for immune system regulation of anterior pituitsary hormone release.
Abstract: Interleukin-6 (IL-6), a cytokine produced by inflammatory reactions, was found to stimulate PRL, GH and LH release from anterior pituitary cells at concentrations similar to those which affected lymphocyte mitogenesis. Perifused pituitary cells responded to IL-6 with prompt increases in hormone release that declined rapidly following cessation of exposure. Dopamine (DA) attenuated IL6-induced PRL release. In addition, IL-6 potentiated both GHRF- and TRH-induced hormone release without an affect on intracellular cAMP. These data demonstrate a new biological activity for IL-6 and provide evidence for immune system regulation of anterior pituitary hormone release.

330 citations


Journal ArticleDOI
TL;DR: It is found that when the pituitary-specific 33-kD transcription factor Pit-1 is expressed in either the heterologous HeLa cell line or in bacteria, it binds to and activates transcription from both growth hormone and prolactin promoters in vitro at levels even 10-fold lower than those normally present in pituitaries.
Abstract: The anterior pituitary gland provides a model for investigating the molecular basis for the appearance of phenotypically distinct cell types within an organ, a central question in development. The rat prolactin and growth hormone genes are expressed selectively in distinct cell types (lactotrophs and somatotrophs, respectively) of the anterior pituitary gland, reflecting differential mechanisms of gene activation or restriction, as a result of the interactions of multiple factors binding to these genes. We find that when the pituitary-specific 33-kD transcription factor Pit-1, expressed normally in both lactotrophs and somatotrophs, is expressed in either the heterologous HeLa cell line or in bacteria, it binds to and activates transcription from both growth hormone and prolactin promoters in vitro at levels even 10-fold lower than those normally present in pituitary cells. This suggests that a single factor, Pit-1, may be capable of activating the expression of two genes that define different anterior pituitary cell phenotypes. Because a putative lactotroph cell line (235-1) that does not express the growth hormone gene, but only the prolactin gene, appears to contain high levels of functional Pit-1, a mechanism selectively preventing growth hormone gene expression may, in part, account for the lactotroph phenotype.

329 citations


Journal ArticleDOI
15 Jun 1989-Nature
TL;DR: Results indicate that both somatotropes and lactotropes derive from a common GH-expressing stem-somatotrope, which is still present in the adult animal and is capable of repopulating the pituitaries of treated animals with mature GH and Prl producing cells.
Abstract: The pituitary gland, composed of the anterior, intermediate and posterior lobe, represents a principal regulatory interface through which the central nervous system controls body physiology. The ontogeny of the growth hormone (GH) and prolactin (Prl) producing cells of the anterior pituitary has been analysed in transgenic mice, using the thymidine kinase obliteration system (TKO). Cells expressing the herpes virus 1 thymidine kinase (HSV1-TK) gene acquire pharmacological sensitivity to synthetic nucleosides such as FIAU (1-(2-deoxy-2-fluoro-beta-delta-arabinofuranosyl)-5-iodouracil), whose metabolites kill dividing cells. Consequently we created transgenic mice carrying the HSV1-TK gene under the control of either the rat growth hormone or the rat prolactin promoter. If transgenic mice expressing HSV1-TK in somatotropes (GH-producing cells) are treated with FIAU, they develop as dwarfs. The anterior pituitary in these animals is nearly devoid of both somatotropes and lactotropes (Prl-producing cells). By contrast, transgenic mice expressing HSV1-TK in the lactotropes, treated with FIAU, have anatomically and histologically normal pituitaries. Because toxicity depends on cell division, we conclude that Prl expression and lactotrope differentiation are post-mitotic events. These results indicate that both somatotropes and lactotropes derive from a common GH-expressing stem-somatotrope. Unexpectedly, the stemsomatotrope is still present in the adult animal and is capable of repopulating the pituitaries of treated animals with mature GH and Prl producing cells.

314 citations


Journal ArticleDOI
TL;DR: The mirthful laughter experience appears to reduce serum levels of cortisol, dopac, epinephrine, and growth hormone, which have implications for the reversal of the neuroendocrine and classical stress hormone response.

305 citations


Journal ArticleDOI
TL;DR: In the present study rats were dosed from weaning, through puberty and gestation, to Day 15 of lactation with methoxychlor at 25, 50, 100, or 200 mg/kg/day and the fertility of treated males was not reduced when they were mated with untreated females and when the females were bred with untreated or similarly treated males.

272 citations


Journal ArticleDOI
TL;DR: In general, both growth hormone and cortisol levels were elevated when hypoosmoregulatory ability was high and Conversely, prolactin levels generally showed a negative relationship with hypoos moregulatory able.

209 citations


Journal ArticleDOI
TL;DR: It is suggested that a protein with homology to PRL and recognized by these anti‐PRL antibodies is produced by lymphocytes and plays a critical role in their progression through the cell cycle.
Abstract: Recent in vivo studies have shown that treatments that decrease circulating prolactin (PRL) in rodents result in significant immunosuppression. Our attempts to demonstrate corresponding direct stimulatory effects of PRL on cultured lymphocytes were unsuccessful. However, antibodies against pituitary PRL potently inhibited both murine and human lymphocyte proliferation in response to both T and B cell mitogens. Further studies using IL 2 and IL 4 responsive cell lines (CTLL-2 and HT-2) demonstrated that the same anti-PRL antibodies inhibited the proliferative response to these cytokine growth factors. Thus, antibodies to PRL appear to block an event occurring in the G1 to GS phase transition of these cell lines, which constitutively express growth factor receptors. The inhibitory activity of anti-PRL antibodies could be adsorbed by addition of purified human PRL or by immobilized PRL on an affinity column. Antibodies to other pituitary hormones were without inhibitory effect on CTLL-2 cell proliferation. P...

189 citations


Journal ArticleDOI
TL;DR: Two lambda gt11 clones containing fragments of cDNA encoding the prolactin receptor from rabbit mammary gland were isolated using a rat liver prolactIn receptor cDNA probe to establish the sequence identity of this form of prolact in receptor with the growth hormone receptor.
Abstract: Two lambda gt11 clones containing fragments of cDNA encoding the prolactin receptor from rabbit mammary gland were isolated using a rat liver prolactin receptor cDNA probe. An 1848-base-pair open reading frame encodes a mature prolactin-binding protein of 592 amino acids that contains three domains: (i) the extracellular, amino-terminal, prolactin-binding region of 210 residues; (ii) the transmembrane region of 24 residues; and (iii) the intracellular, carboxyl-terminal domain of 358 residues. This latter domain is much longer than the cytoplasmic domain (57 residues) previously described for the rat liver prolactin receptor. In addition, the sequence identity of this form of prolactin receptor with the growth hormone receptor is extended in the cytoplasmic domain.

Journal ArticleDOI
TL;DR: Data indicate that growth hormone may play an important role in the development of hypoosmoregulatory activity and increased hypoos moregulatory ability also appears to be associated with low prolactin levels.

Journal ArticleDOI
TL;DR: It is concluded that pituitary-adrenal activation in response to Il-1 is caused by CRF secretion from a subtype of CRF neurons (not storing AVP) in the rat hypothalamus.
Abstract: Effects on turnover of vasopressin (AVP) in the hypothalamus and on secretion of pituitary hormones, catecholamines and insulin after intraperitoneal injection of recombinant interleukin-1 (beta) (IL-1) were investigated in male wistar rats. Intraper-itoneal administration of IL-1 in a dose (1 µg) that maximally activated pituitary-adrenal activity failed to alter plasma concentrations of prolactin, luteinizing hormone and melanocyte-stimulating hormone. Rats chronically cannulated in the right jugular veins showed a time-related increase in plasma corticosterone concentrations in response to intraperitoneal administration of IL-1 that lasted up to 4 h. In the same rats, plasma epinephrine (E) and norepinephrine (NE) concentrations were only slightly elevated (2-fold increase) at 30 min and at 1 h after IL-1 administration. Unlike in endotoxin-resistant C3H/HeJ mice, where IL-1 induces hypoglycemia, IL-1 did not affect plasma concentrations of glucose and insulin in Wistar rats. In the zona externa of the median eminence, IL-1 stimulated corticotropin-releasing factor (CRF) turnover at an approximate rate of 15%/h, but did not cause a concomitant change in AVP turnover as can be observed after insulin-induced hypoglycemia. Since half of the hypothalamic CRF neurons have been shown to costore AVP, the data favor the view of a selective effect of IL-1 on a subtype of CRF neurons. We conclude that pituitary-adrenal activation in response to II-1 is caused by CRF secretion from a subtype of CRF neurons (not storing AVP) in the rat hypothalamus. Furthermore, the small and transient increase of plasma E and NE may be caused by a presynaptic action of IL-1 on sympathetic nerves in immune and/or other organs or may involve central CRF projections regulating sympathetic outflow.

Journal ArticleDOI
TL;DR: Dietary restriction in the developing female lamb depresses gonadotropin secretion without reducing other anterior pituitary gland secretions, such as PRL and GH, which implies that metabolic and growth-related modulation of neuroendocrine function can occur independently of changes in sensitivity to the feedback actions of ovarian steroids and polypeptides.
Abstract: The acute and long term effects of dietary restrictions on gonadotropin secretion were studied in ovariectomized female lambs Nutritionally growth-restricted lambs which were chronically maintained at a body weight comparable to that at weaning (∼20 kg) became hypogonadotropic, exhibiting a low frequency of episodic LH discharges Repeated administration of physiological doses of GnRH to these females at hourly intervals produced corresponding LH pulses, leading to the hypothesis that the dietary-induced hypogonadotropism arises from a deficiency in endogenous GnRH release, rather than an inability of the pituitary gland to secrete gonadotropins in response to hypothalamic stimulation In such growth-restricted females receiving a single meal daily, initiation of ad libitum feeding led to a spontaneous LH pulse within 1 h After 14 days of increased food intake, hourly LH pulses were evident; a marked reduction in LH pulse frequency was associated with the return to limited nutrition No effects

Journal ArticleDOI
TL;DR: Evidence indicates that the inhibitory effects of nicotine on LH and prolactin secretion are produced via an activation by these nicotinic receptors of the tubero-infundibular dopamine neurons, releasing dopamine as a Prolactin inhibitory factor.

Journal ArticleDOI
TL;DR: Findings show that the pituitary gland directly affects TEC in terms of cytoskeletal and secretory protein expression as well as cell cycle, and the effects of PRL on TEC were not restricted to thymic hormone production.
Abstract: The thymic epithelium is responsible for the secretion of thymic peptides, which intervene in some steps of intra- and extrathymic T cell differentiation. Recent data suggest that thymic hormone secretion is modulated by the neuroendocrine network, comprising thyroid, adrenals, and gonads. However, the role of the pituitary gland in this regulation is still poorly understood. In the present paper we studied the in vivo and in vitro influences of PRL on the secretion of thymulin, one of the chemically defined thymic hormones, by thymic epithelial cells (TEC). When injected daily (20-100 micrograms/20 g) in young or old C57BL/6 mice, PRL induced a specific increase in thymulin synthesis and secretion, respectively, measured by the number of thymulin-producing cells in the thymus and the peripheral levels of the hormone. This stimulation was dose dependent and reversible after the end of treatment. Similar findings have been made in animals with pituitary dwarfism, known to have low levels of circulating thymulin. This stimulatory effect was also observed in primary cultures of human and mouse TEC when PRL (10(-7) to 10(-8) M) was applied to culture supernatants, thus suggesting that PRL could act directly on TEC. In addition, we induced in vivo experimental hypoprolactinemia, treating mice with bromocriptine, a dopamine receptor agonist that inhibits pituitary PRL secretion. Bromocriptine treatment (100-200 micrograms/20 g) yielded a significant decrease in thymulin secretion that could be reversed by coincident treatment with PRL. In the light of previous observations that bovine GH can also increase thymulin production in aged dogs, we performed a series of experiments in vitro to evaluate whether GH has a direct effect on TEC. We observed that only human GH preparations that are known to have a PRL-like effect were efficient in stimulating thymulin biosynthesis and release into the culture supernatants. The effects of PRL on TEC were not restricted to thymic hormone production. We observed that TEC proliferation, as well as the numbers of a TEC subset defined by the expression of cytokeratins 3 and 10, could also be increased by PRL treatment. All these findings show that the pituitary gland directly affects TEC in terms of cytoskeletal and secretory protein expression as well as cell cycle.

Journal ArticleDOI
TL;DR: The correlation between serum levels of PRL and the expression of PTH-LP mRNA in mammary tissue extends the role ofPRL in milk production and suggests a possible mechanism for the PRL effects on calcium metabolism.
Abstract: During lactation, a dramatic rise in serum PRL stimulates milk production, resulting in a substantial rise in calcium mobilization from gut and bone. We found that the production of a newly characterized calcium-mobilizing PTH-like peptide (PTH-LP) by mammary tissue was tightly linked to lactation, suggesting a possible role for PRL in the expression of PTHLP. Here it is shown that suckling results in both an elevation in serum PRL and the appearance of PTHLP mRNA in mammary tissue. Bromocriptine, a potent inhibitor of PRL secretion, blocked the sucklingassociated rise in serum PRL and the subsequent induction of PTH-LP mRNA in mammary gland. Furthermore, injection of PRL dramatically induced PTHLP mRNA in unsuckled puerperal glands, but not in glands on day 21 of pregnancy. Thus, the correlation between serum levels of PRL and the expression of PTH-LP mRNA in mammary tissue extends the role of PRL in milk production and suggests a possible mechanism for the PRL effects on calcium metabolism.

Journal ArticleDOI
TL;DR: This review discusses the possible physiological importance of milk contains a significant number of substances having peptide characteristics that are known to possess biological activity on suckling mammals after gastrointestinal administration.
Abstract: Milkcontains a significant number of sub stances having peptide characteristics that are known to possess biological activity. The possible physiological im portance for the neonate is discussed in this reviewin light of their effects (epidermal growth factor, nerve growth fac tor, insulin, prolactin, somatostatin, thyroid-releasing hor mone, thyroid-stimulating hormone, growth hormoneâ€"re leasing factor, luteinizing hormone-releasing hormone, adrenocorticotrophic hormone, erythropoietin, bombesin- like peptides, calcitonin, AŸ-casomorphinsand delta-sleep- peptides) on suckling mammals after gastrointestinal administration. J. Nutr. 119: 1543-1551, 1989.

Journal ArticleDOI
TL;DR: Female subjects demonstrated a more robust increase in plasma prolactin following L-TRP infusion pre-diet and exhibited a larger decrease in plasma TRP following dietary TRP restriction compared to males, suggestive of postsynaptic serotonin receptor supersensitivity.

Journal ArticleDOI
TL;DR: Complete or partial sequencing of several milk protein genes and comparative analysis have led to identification of a sequence of high homology and conservation in the 5' flanking region that is likely to be involved in the regulation of milk protein gene expression.
Abstract: Growth and differentiation of the mammary gland are controlled by various hormones and other environmental factors. The role of hormones and growth factors in mammary development is discussed with regard to animal species, physiological stages, and the various experimental systems in vitro. In the female embryo, mammary morphogenesis is induced by the mesenchyme and is hormone independent, whereas androgens cause the partial necrosis of mammary epithelium in the male. Ductal growth during adolescence requires estrogen and prolactin or growth hormone. During pregnancy, progesterone participates in the development of the lobuloalveolar structure of the gland. After parturition, changes in the hormonal environment lead to production and secretion of milk. Proliferation and differentiation of mammary epithelium can be induced in culture systems. Insulin and epidermal growth factor (EGF) stimulate mammary cell proliferation in vitro. EGF is required for the optimal growth of the mammary gland during pregnancy. EGF also appears to play an important role in mammary tumorigenesis in certain mouse strains. Production of milk proteins can be induced in vitro by the synergistic interactions of prolactin, insulin, and glucocorticoids and is inhibited by EGF and progesterone. Complete or partial sequencing of several milk protein genes and comparative analysis have led to identification of a sequence of high homology and conservation in the 5' flanking region that is likely to be involved in the regulation of milk protein gene expression.

Journal ArticleDOI
TL;DR: The discovery of the ability of prolactin and growth factors to activate nuclear protein kinase C may constitute a breakthrough in the understanding of how these hormones regulate trophic responses.

Journal ArticleDOI
TL;DR: Thyroid hormone treatment specifically suppressed alpha-subunit and TSH beta mRNA synthesis, indicating that the culture system is responding in an appropriate physiological manner and that decreases in transcription can be easily and accurately measured with this system.
Abstract: Our previous work demonstrated that in vivo estradiol (E2) administration to ovariectomized rats suppressed the transcription of the LH subunit genes within 4 h. To determine whether these effects were mediated directly at the level of the gonadotrope, the transcription rates of the LHβ, FSHβ, and α-subunits were measured in short term cultures of pituitary fragments from female rats in various physiological states. In each in vitro experiment, fragments from matched sets of hemipituitaries were used for control and treatment (10−8mE2) groups. In pituitaries from ovariectomized animals, treated in vitro with or without E2, there was no significant effect of 2 h or 6 h of E2 on FSHβ or α-subunit gene transcription, but a consistent 2- to 3-fold stimulation of LHβ mRNA synthesis. In pituitaries from intact randomly cycling rats, E2 in culture had no effect on the transcription rate of α-subunit, FSHβ, or TSHβ genes, but stimulated LHβ and PRL transcription 2- fold. Thyroid hormone treatment specifically sup...

Journal ArticleDOI
TL;DR: The findings on the membrane receptors in the human and rat prostate cancers raise the intriguing possibility that LH‐RH, acting as a growth factor, along with EGF and prolactin, might be involved in complex interactions that contribute to the promotion of prostate cancer in man.
Abstract: Using sensitive multipoint micromethods, we estimated membrane receptors for [D-Trp6]-luteinizing hormone-releasing hormone ([ D-Trp6]-LH-RH), somatostatin (SS-14), human prolactin (hPRL), and epidermal growth factor (EGF) in experimental Dunning rat prostate cancers and in samples of normal human prostate, benign prostatic hyperplasia (BPH), and human prostate cancer (PC) obtained from biopsy, after prostatectomy, or at autopsy. In the Dunning R-3327 rat prostate adenocarcinoma specimens, the receptors were characterized in untreated animals and following in vivo treatment with microcapsules of the agonist [D-Trp6]-LH-RH and the somatostatin analog RC-160. Two populations of binding sites were found for [D-Trp6]-LH-RH, one with high affinity and low capacity and another with low affinity and high capacity. Treatment with [D-Trp6]-LH-RH and RC-160 alone or with the combination of these analogs increased the binding capacity (Bmax) of the low-affinity binding sites for [D-Trp6]-LH-RH and decreased Bmax for hPRL and EGF. Therapy with [D-Trp6]-LH-RH also reduced Bmax of SS-14 binding and dissociation binding constant of high-affinity binding sites for [D-Trp6]-LH-RH, whereas administration of RC-160 or the combination treatment with both analogs increased Bmax of SS-14 binding. These findings are compatible with the view that analogs of LH-RH and SS-14 might exert some direct inhibitory effects on the Dunning prostate cancer. Among 13 human BPH samples examined, only one had receptors for [D-Trp6]-LH-RH, and seven specimens exhibited binding for prolactin. [D-Trp6]-LH-RH receptors were found in all seven samples of human PC but not in any of the eight specimens of normal human prostate. All samples of normal human prostate, BPH, and human PC exhibited binding sites for EGF but not for SS-14. Our findings on the membrane receptors in the human and rat prostate cancers raise the intriguing possibility that LH-RH, acting as a growth factor, along with EGF and prolactin, might be involved in complex interactions that contribute to the promotion of prostate cancer in man.

Journal ArticleDOI
TL;DR: The results suggest that at least part of the stimulatory action of the peptide on pituitary hormone release is brought about by prostaglandins.
Abstract: Cachectin (tumor necrosis factor) is a powerful macrophage hormone released during infection, which circulates in blood to produce diverse effects in the organism. We examined the effect of cachectin on release of anterior pituitary hormones from either hemipituitaries or dispersed pituitary cells incubated in vitro. The action of cachectin on dispersed cells was demonstrable only after 2 hr of incubation. With this incubation time, the protein produced a dose-related stimulation of release of adrenocorticotropin (ACTH), growth hormone (GH), and thyrotropin (TSH), but not of prolactin (Prl), from both hemipituitaries and dispersed cells. The doses required for stimulation were low in the case of hemipituitaries, usually of the order of 10(-12) M, whereas they were higher by one or two orders of magnitude with the dispersed pituitary cells. This may be related either to loss of receptors for the protein during the dispersion procedure or to the fact that in the hemipituitary system cell interactions are facilitated because the cells are close to each other. In the dispersed cell system cachectin evoked a dose-related decrease in cyclic AMP content. Incubation with somatostatin lowered the cyclic AMP content of the cells and depressed GH output without altering output of TSH or Prl. When somatostatin and cachectin were incubated together with the cells, the suppression of cyclic AMP production was abolished; TSH and Prl release were stimulated, but the action of cachectin to stimulate GH release was blocked. The stimulation of Prl release by cachectin in the presence of somatostatin may be related to the elevation of cyclic AMP, a known stimulator of Prl release. The cyclooxygenase inhibitor indomethacin nearly completely blocked the stimulatory effect of cachectin on release of GH and TSH from dispersed pituitary cells but had only a slight and nonsignificant attenuating effect on its ACTH-releasing action. These results suggest that at least part of the stimulatory action of the peptide on pituitary hormone release is brought about by prostaglandins. The failure of indomethacin to block the release of ACTH induced by cachectin suggests that other mechanisms may be involved in the release of ACTH induced by this peptide. Since the concentrations of cachectin required to stimulate pituitary hormone release are similar to those that are encountered in plasma during infection, it is likely that this direct pituitary action has pathophysiological significance.

Journal ArticleDOI
TL;DR: The simultaneous elevation of serum prolactin, thyrotropin, growth hormone, and cortisol points to a central stimulation of the hypothalamic-pituitary axis during an epileptic seizure, but not during seizures of psychogenic origin.
Abstract: The circadian rhythm of serum prolactin was determined in 12 patients with seizures, and 28 age- and sex-matched healthy subjects (14 men and 14 women). Blood was also collected every 15 min for 2 h i

Journal ArticleDOI
TL;DR: The data indicate that elevated prolactin levels stimulate food intake in a dose-dependent manner and that this hyperphagia is not accompanied by an increase in BAT mitochondrial GDP binding.
Abstract: Lactation in the rat is marked by pronounced hyperphagia and suppression of brown fat (BAT) thermogenic capacity. We previously examined the possibility that elevated prolactin levels mediate these changes. The present study evaluated the effect of varying prolactin levels on food intake, BAT mitochondrial GDP binding, and carcass adiposity. Female rats were injected daily for 10 days with ovine prolactin at one of three doses: high = 3.0, medium = 1.0, or low = 0.3 micrograms/g body wt. Controls were injected with 0.9% NaCl. A group of uninjected rats served as an additional control. Cumulative food intake was significantly elevated in a dose-dependent manner in the prolactin-treated animals relative to the saline-injected and uninjected controls. Compared with the saline controls, the mean cumulative food intake was greatest at the high dose (20% increase), intermediate at the medium dose (17%), and smallest at the low dose (12%). Prolactin-treated rats gained significantly more weight during the experiment than did controls. Despite the hyperphagia in the prolactin-treated rats, no significant differences in BAT mitochondrial GDP binding were observed among the five groups. These data indicate that elevated prolactin levels stimulate food intake in a dose-dependent manner and that this hyperphagia is not accompanied by an increase in BAT mitochondrial GDP binding.

Journal ArticleDOI
15 Jul 1989-Cancer
TL;DR: A positive correlation existed between the nocturnal melatonin peak and progesterone and androgen receptor concentrations in primary tumors indicating a direct involvement of melatonin in the growth control of breast cancer.
Abstract: Serum melatonin was determined over 24 hours in 35 patients with breast cancer with either a fresh primary tumor (n = 23) or a secondary tumor (n = 12) and in 28 patients with untreated benign breast disease (controls) having a fibroadenoma (n = 10), fibrocystic mastopathy (n = 14), or other breast diseases (n = 4). Circadian rhythms existed in all groups with acrophases at 2 a.m. A 50% depression of peak and amplitude occurred in the group of patients with primary breast cancer compared with age-matched controls (P less than 0.001, P less than 0.01). The peak declined with increasing tumor size: 27% at Stage T1, 53% at T2 (P less than 0.001), and 73% at T3 (P less than 0.05). In contrast, patients with secondary breast cancer, particularly those receiving antiestrogen therapy, had a melatonin peak similar to controls. These results demonstrated a transient depression of pineal melatonin secretion in primary breast cancer and indicated a dynamic role of the pineal gland in malignancy. To investigate some endocrine effects of a depressed melatonin peak, the 24-hour rhythms of prolactin (PRL) and thyroid stimulating hormone (TSH) were determined in patients with primary breast cancer and compared with patients with secondary breast cancer. The PRL had significant circadian rhythms in both groups; but acrophases occurred at midnight in patients with secondary breast cancer, and there were unusually high concentrations at noon in patients with primary breast cancer. Circadian rhythms were not seen for TSH, but the 24-hour average secretion was depressed by 45% (P less than 0.01) in patients with primary breast cancer. The abnormal concentrations of PRL and TSH in these patients could be due to a depressed melatonin peak normally serving as a central circadian synchronizer and modulator of the secretion of adenohypophysial hormones. Additionally, a positive correlation existed between the nocturnal melatonin peak and progesterone and androgen receptor concentrations in primary tumors indicating a direct involvement of melatonin in the growth control of breast cancer.

Journal ArticleDOI
TL;DR: Data indicate that differing therapies may be appropriate for depression in breast- and bottle-feeders, and significant correlations were seen between depression ratings and salivary progesterone and prolactin.
Abstract: The incidence of post-natal depression is high, and dramatic changes in steroid hormones and prolactin occur in the post-partum period In an attempt to correlate these events, 147 mothers, six to eight weeks after delivery of a healthy infant, completed standard psychological tests, including the Edinburgh, Montgomery-Asberg, and Raskin scales They also provided matched samples of plasma for assay of cortisol, oestradiol, progesterone and prolactin, and saliva for assay of cortisol and progesterone All steroid concentrations were within the appropriate normal ranges Of the mothers, 149% were depressed on all three scales Significant correlations were seen between depression ratings and salivary progesterone and prolactin In bottle-feeders, salivary progesterone was positively associated with depression, whereas in breast-feeders it was negatively associated Plasma prolactin levels were inappropriately low in depressed breast-feeders These data indicate that differing therapies may be appropriate for depression in breast- and bottle-feeders

Journal ArticleDOI
TL;DR: This hypothesis that the catecholaminergic structures in the L-RCh mediate the inhibition of pulsatile LH secretion by estradiol in the anestrous ewe is tested by injecting 6-hydroxydopamine (6OH-DA) into the L -RCh of ovariectomized ewes and comparing the secretion of LH and prolactin in these animals with that in sham and control animals.
Abstract: Separate studies with ewes have shown that catecholamines play an inhibitory role in the control of LH secretion during anestrus, and that there are structures in the lateral retrochiasmatic area (L-R

Journal ArticleDOI
TL;DR: The emerging picture is that GnRH, oxytocin, A-MSH and substance P stimulate, while CRF, beta-endorphin, prolactin, and neuropeptide Y are inhibitory, which may be relevant to the low level of sexual motivation in some depressed men.