Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of single and repeated doses of met-enkephalin (Met-E) on the ultrastructure and TSH-like immunoreactivity (IR) of pituitary TSH-producing cells, and TSH plasma levels in male rats and the influence of pretreatment with a dopamine antagonist, haloperidol, on these, were evaluated. Both acute and repeated Met-E administration produced changes in TSH cells consisting of: an increase in TSH-like IR, enlargement and dilation of RER and Golgi apparatus, size-increase of secretory granules, and the presence of a variable number of cytoplasmic vacuoles. The ultrastructural changes were more evident in the chronically treated animals, whereas no differences were found in IR-intensity between both Met-E treated groups. Haloperidol alone modifies neither ultrastructure nor TSH-like IR of TSH producing cells, but it prevented the Met-E produced changes. On the other hand, Met-E treatment resulted in a decrease of TSH plasma levels, but being significant only in the acutely injected animals. No variations were produced by haloperidol alone, but it prevented the decrease of TSH plasma levels stimulated by Met-E. Our results suggest that Met-E plays a role in the release of TSH, and that dopamine is implicated in this process. The possible mechanisms through which Met-E influences TSH secretion are discussed.
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PMID:Study of the rat TSH-producing cells after met-enkephalin treatment: effects of dopamine antagonists. 176 27

Several monokines, proteins secreted by monocytes and macrophages, alter release of hormones from the anterior pituitary. We report here the ability of femtomolar concentrations of interleukin 2 (IL-2), a lymphokine released from T lymphocytes, to alter directly pituitary hormone release. The effects of concentrations of IL-2 ranging from 10(-17) to 10(-9) M on anterior pituitary hormone release were evaluated in vitro. Hemipituitaries were preincubated in 1 ml of Krebs-Ringer bicarbonate buffer (KRB) followed by incubation for 1 or 2 hr with KRB or KRB containing different concentrations of IL-2. This was followed by incubation for 30 min in 56 mM potassium medium to study the effect of pretreatment with IL-2 on subsequent depolarization-induced hormone release. Prolactin (PRL), luteinizing hormone (LH), follicle-stimulating hormone (FSH), corticotropin (ACTH), growth hormone (GH), and thyrotropic hormone (TSH) released into the incubation medium were measured by radioimmunoassay. IL-2 stimulated the basal release of PRL at 1 or 2 hr but suppressed the subsequent depolarization-induced PRL release, perhaps because the readily releasable pool of PRL was exhausted. The minimal effective dose (MED) was 10(-15) M. Conversely, IL-2 significantly suppressed the basal release of LH and FSH at 1 or 2 hr, with a MED of 10(-16) M, thus demonstrating a reciprocal action of the cytokine on lactotrophs and gonadotrophs. The subsequent depolarization-induced release of LH and FSH was suppressed, indicative of a persistent inhibitory action of IL-2. IL-2 stimulated ACTH and TSH release at 1 hr and the MEDs were 10(-12) and 10(-15) M, respectively. Conversely, IL-2 significantly lowered the basal release of GH at 1 hr, with a MED of 10(-15) M. The release of GH was not altered at 2 hr. The high potassium-induced release of ACTH, TSH, and GH was not affected. The results demonstrate that IL-2 at picomolar concentrations affects the release of anterior pituitary hormones. This cytokine may serve as an important messenger from lymphocytes exerting a direct paracrine action on the pituitary by its release from lymphocytes in the gland or concentrations in the blood that reach the gland may be sufficient to activate it.
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PMID:Anterior pituitary hormone control by interleukin 2. 184 83

Intravenous interleukin-2 (IL-2) administration has been shown to influence several hormonal secretions. The present study was carried out to investigate the endocrine effects of subcutaneous therapy with IL-2. Six patients with advanced renal cancer were studied. They were treated subcutaneously with IL-2 according to the schedule proposed by Atzpodien et al. Venous blood samples were collected at O-time and 1, 8 and 12 hours after the first IL-2 pulse of 9 X 10(6) IU/m2 at 8.00 a.m.; on a separate occasion, samples were collected during a saline infusion only. In each blood sample, serum levels of cortisol, beta-endorphin, GH, PRL, FSH, LH, TSH and the pineal hormone melatonin were measured by RIA. Both cortisol and beta-endorphin significantly increased after IL-2 injection. GH rose but not to a significant extent. PRL, FSH, LH and TSH did not change after IL-2. Finally, melatonin levels markedly decreased after IL-2 injection in the only 2 patients with elevated concentrations of this hormone before the start of immunotherapy. These results suggest that the endocrine effects of subcutaneous IL-2 therapy are similar to those previously described with intravenous administration.
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PMID:Neuroendocrine effects of subcutaneous interleukin-2 injection in cancer patients. 186 47

The adrenocorticotropin-releasing effect of arginine vasopressin is well known. The effects of AVP on other anterior pituitary hormones remain confusing, with few in vivo human data available. Two human studies of exogenous AVP effects on ACTH, GH, TSH and prolactin are described. In the dosage and route of administration used, AVP was found to be a specific ACTH secretagogue.
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PMID:Human anterior pituitary response to exogenous arginine vasopressin. 195 56

Hypothalamic pituitary functions were studied in 25 patients before and 6 months after cranial irradiation with or without radiosensitizing chemotherapy for nasopharyngeal carcinoma. The estimated average total dose was 5,000 cGy to the hypothalamus and pituitary gland. The radiosensitizing chemotherapy used was endoxan, 4900 +/- 873 mg and/or methotrexate 113 +/- 30 mg. All patients had normal pituitary function before radiotherapy. Six months after radiotherapy, there was a significant increase in baseline serum thyrotropin (TSH) and follicle-stimulating hormone (FSH) levels. The TSH response to thyrotropin-releasing hormone (TRH) was significantly increased, suggesting primary hypothyroidism due to neck irradiation. The peak serum TSH response to TRH became delayed in 21 patients, suggesting a defect in TRH release. In male patients who did not receive radiosensitizing chemotherapy, the FSH response to luteotropic hormone-releasing hormone (LHRH) increased while the luteinizing hormone (LH) response decreased. But in male patients who also received radiosensitizing chemotherapy, both the FSH and LH responses to LHRH increased. The adrenocorticotropic hormone (ACTH) response to ovine corticotropin-releasing hormone (CRH) did not change, while the integrated cortisol response increased. The growth hormone (GH) response to growth hormone-releasing hormone (GRH) did not change. The GH response to insulin tolerance test (ITT) increased and may be explained by the more severe hypoglycemia induced by the same dosage of insulin after radiotherapy or the recovery from the previous wasting caused by radiotherapy. There was no significant increase in serum prolactin. In conclusion, we demonstrated impairment of the hypothalamus-pituitary-endocrine gland axes as early as 6 months after cranial irradiation with or without chemotherapy.
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PMID:Early effects of cranial irradiation on hypothalamic pituitary function. 197 95

Factors associated with heat-induced increase in blood prolactin (PRL) were investigated. Ten male volunteers (23.7 +/- 2.2 yr) were exposed to exogenous heating (head-out immersion) in 41 degrees C water (control 37 degrees C) for 30 min with and without face fanning and cooling. In seven of the subjects, endogenous heating was produced by a 45-min exercise in a warm environment (41 degrees C; control 10 degrees C) with and without selective face fanning. Venous blood was collected before and after each trial; blood hormones were analyzed by radioimmunologic techniques. Heat loading, whether exogenous or endogenous in origin, induced significant increases in blood PRL, beta-endorphin, and vasoactive intestinal peptide (VIP) levels. Blood thyrotropin (TSH) level decreased significantly during water immersion and more significantly with face cooling. From measurement in peripheral blood, the differential beta-endorphin, VIP, and TSH responses to selective face ventilation during exogenous and endogenous heat exposures suggest that blood PRL released in heat derives from secretory stimuli that are independent of these prolactinotropic factors.
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PMID:Prolactinotrophic effect of endogenous and exogenous heat loads in human male adults. 203 3

The neurotransmitter histamine participates in the neuroendocrine regulation of pituitary hormone secretion by an indirect action at a hypothalamic level where histaminergic neurons are abundant. The effect of histamine is caused by activation of postsynaptic H1- or H2-receptors. Histamine stimulates the secretion of ACTH, beta-endorphin (mediated by CRH and AVP), alpha-MSH (mediated by dopamine and peripheral catecholamines), and PRL (mediated by dopamine, serotonin and AVP), and participates in the stress-induced release of these hormones and possibly in the suckling- and estrogen-induced PRL release. The release of GH and TSH is predominantly inhibited by histamine; however, uncertainty exists regarding its role and the hypothalamic factors involved. Histamine increases the secretion of LH in females (mediated by GnRH), and may be involved in the mediation of the estrogen-induced LH surge. AVP and oxytocin are stimulated by histamine, probably by an effect in the supraoptic and paraventricular nuclei of the hypothalamus.
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PMID:The role of histamine in the neuroendocrine regulation of pituitary hormone secretion. 206 91

Opioid peptides and catecholamines play an important role in the control of appetite, behaviour and hormonal secretion. To evaluate the role of the opioid and adrenergic systems in the hormonal dysfunction of anorexia nervosa (AN), we investigated the effects of naloxone and clonidine on serum GH, LH, FSH, beta-endorphin, TSH, prolactin and cortisol concentrations in 35 women with AN. Basal plasma beta-endorphin concentrations were significantly lower than those in healthy controls. The response of beta-endorphin to clonidine in the AN patients was increased, whereas the response of beta-endorphin to naloxone was decreased. Basal serum cortisol concentrations were significantly higher in the AN patients than that in the controls. There was a significant increase in the cortisol response to naloxone in the controls but a lack of cortisol response to naloxone in the patients with AN. Naloxone produced a significant increase in LH release in the controls during the luteal phase of the menstrual cycle, as well as in the majority of AN patients. Clonidine caused a diminution of LH in the controls and did not alter LH in the patients. After clonidine injection, a significant increase in GH release was observed in both groups of subjects. If these disturbances persist after normalization of body weight, it might suggest that altered opioid and adrenergic activity is an aetiological factor in the pathogenesis of anorexia nervosa.
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PMID:Are disturbances in opioid and adrenergic systems involved in the hormonal dysfunction of anorexia nervosa? 212 11

A 44-yr-old man with hypocortisolism was shown to have an undetectable basal plasma ACTH level and absent or subnormal ACTH and beta-lipotropin responses to provocative testing with insulin, vasopressin, and CRH. Endocrine function after glucocorticoid replacement was otherwise normal, thus establishing the diagnosis of isolated ACTH deficiency. This patient's serum was tested immunohistochemically for the presence of an antipituitary antibody by indirect immunofluorescence of rat pituitary tissue. Positive immunostaining was observed in stellate-shaped cells in the anterior and intermediate lobes. Immunopositive cells were shown by immunoelectron microscopy to have ultrastructural characteristics of corticotrophs. Immunoreactivity was concentrated in secretory granules 120-170 nm in diameter. In a double immunolabeling procedure, staining by the patient's serum was shown to colocalize with rabbit antiserum to ACTH, but not with antisera to PRL, GH, beta TSH, or beta LH. Immunoabsorption of the patient's serum with ACTH-(1-24), ACTH-(1-39), gamma MSH, corticotropin-like intermediate lobe peptide, beta-endorphin, or beta-lipotropin failed to diminish immunolabeling in the pituitary. We conclude that the antipituitary antibody in this patient's serum shows immunohistochemical specificity for a rat corticotroph antigen located in secretory granules that is neither ACTH nor any of the proopiomelanocortin (POMC)-derived peptides tested. The autoantigen could be a cell-specific granular factor involved in the posttranslational processing of POMC or secretion of ACTH. We postulate that an autoimmune process may account for this patient's disease, and that his antipituitary antibody could play a pathogenic role by either inhibiting a POMC-processing enzyme or initiating an antibody-dependent cell-mediated cytotoxicity reaction, resulting in the selective destruction of corticotrophs.
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PMID:Isolated adrenocorticotropin deficiency associated with an autoantibody to a corticotroph antigen that is not adrenocorticotropin or other proopiomelanocortin-derived peptides. 215 84

Cold stress stimulates the release of both ACTH and TSH from the pituitary. More striking changes in ACTH content have been seen in the intermediate lobe after cold stress. Therefore, this study was designed to test responses of individual anterior lobe corticotropes to cold exposure. Male rats were exposed to either 30 min of cold (+3-5 C), 30 min of a novel, temperate environment (+24 C) or were unstressed (+24 C). Pituitaries were fixed and embedded in preparation for immunolabeling for ACTH or TSH-beta at the light (semithin sections) and electron microscopic levels. The semithin sections were used to measure areas of corticotropes and thyrotropes with Bioquant image analysis equipment. Separate groups of pituitaries were dissociated and the cells were cultured for 2 or 15 h. Then the cells were stimulated for 5-10 min with biotinylated analogs of corticotropin-releasing hormone (bio-CRH) or arginine vasopressin (bio-AVP) to detect the target cells cytochemically. A third group of dissociated cells were fixed for immunolabeling for ACTH, 16K fragment of pro-opiomelanocortin, beta-endorphin, or TSH-beta. Cold exposure resulted in a 1-4-fold increase in the levels of serum ACTH over that of unstressed rats. This was correlated with a 40% increase in the percentage of cells that contained 16K fragment and a 30-40% increase in percentages of cells storing ACTH or beta-endorphin. Cold stress also increased the percentage of cells that bound bio-CRH or bio-AVP by 45%. Analyses of semithin sections showed that areas of corticotropes increased by 21% following cold stress. The number of rows of immunolabeled (ACTH) secretion granules also increased in corticotropes from cold-stressed rats. Exposure to a novel environment for 30 min resulted in no significant increase in serum ACTH over that of unstressed rats. There was, however, a 20% increase in percentages of cells that stored 16K fragment, beta-endorphin, or target cells that bound bio-CRH. However, the corticotropes were not significantly larger. Many of the cells exhibited reduced numbers of immunolabeled secretory granules. Other corticotropes resembled those from cold-stressed rats. When TSH cells were studied, their percentages increased from 8 +/- 3% to 15.8 +/- 4% and their areas increased by 22% following exposure to cold. After exposure to a novel environment, percentages of cells that stored TSH-beta increased to 11 +/- 2%, however, no changes in areas of TSH cells were measured. These studies demonstrated that the anterior lobe corticotrope is clearly activated by exposure to both cold and novel environment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cytochemical studies of responses of corticotropes and thyrotropes to cold and novel environment stress. 216 13


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