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)

Previous studies have indicated that acute stress in vivo or ovine corticotropin releasing hormone (oCRH) in vitro, releases both beta-lipotropin (beta-LPH) and beta-endorphin (beta-END) from the anterior lobe, with beta-END predominating over beta-LPH by 2:1. However, repeated stress shifts this ratio to proportionately more beta-LPH released with re-stress or oCRH in vitro. Alternative hypotheses were that the glucocorticoids released during stress altered the processing of proopiomelanocortin (POMC) or that the increased biosynthetic drive resulted in an inability of the processing enzymes to keep pace with biosynthesis. To distinguish between these alternatives, adrenalectomy studies were performed. Following removal of glucocorticoid negative feedback there is greatly increased secretion of beta-END-IR from anterior lobe corticotrophs with a subsequent increase in biosynthetic drive. Under these conditions of increased biosynthetic drive in the absence of steroids, the corticotroph secretes primarily beta-LPH, suggesting that increased biosynthetic drive alters the posttranslational processing rate of POMC.
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PMID:Adrenalectomy increases beta-lipotropin secretion over beta-endorphin secretion from anterior pituitary corticotrophs. 260 76

Hemidecortication (HD) (left cerebral hemisphere) was performed in rats with the aim of analyzing the modulating effect of the cerebral cortex on the hypothalamic-pituitary-adrenal axis. Corticosterone release induced either by ether or immobilization stress was evaluated in control (C) and HD rats. The percentage increase in corticosterone was greater in HD than in C rats after 15 min of ether stress (HD = 142%, C = 50%) and after 60 min of immobilization stress (HD = 197%, C = 126%). An in vitro test showed that the release of ACTH induced by corticotropin releasing hormone (CRH) from hemipituitary fragments from HD rats was not different from that in control rats. These results suggest an inhibitory effect of the cerebral cortex on the hypothalamus which may modulate the secretion of corticotropin releasing peptides.
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PMID:Ether and immobilization stress effects on pituitary adrenal function in hemidecorticate rats. 262 Jan 93

Male rats were exposed to severe 14 day immobilization stress. Body weight, body temperature, food and water intake, behavioral parameters, and serum corticosterone levels were measured during and after the stress period. On the 7th day after cessation of stress the experimental animals together with the control rats were taken to immunocytochemical analysis involving morphometry and microdensitometry of tyrosine hydroxylase (TH), 5-hydroxytryptamine (5-HT), various neuropeptide, and glucocorticoid receptor (GR) immunoreactivities (IRs) in a large number of regions of the central nervous system. In addition, adrenocorticotropic hormone (ACTH) IR was analyzed in the pituitary gland. Seven days following cessation of the chronic stress food intake, total locomotion and forward locomotion had been restored to normal. Serum corticosterone levels appeared to remain increased even 6 days following cessation of the chronic immobilization stress, probably caused by increased release of ACTH. Paraventricular corticotropin releasing hormone (CRF) IR was negatively correlated with the pituitary ACTH IR, indicating that the increase in ACTH release was produced by an increased release of CRF from the hypothalamus. The major immunocytochemical change observed 7 days after cessation of stress was a disappearance of 5-HT IR in the 5-HT cell groups B1, B2, B3, and B7. 5-HT IR in nerve terminals was only affected in the dorsal horn, where 5-HT IR was increased in the substantia gelatinosa. GR IR was found to be significantly increased in monoaminergic cell groups: serotoninergic B7, dopaminergic A12, and noradrenergic A1, A2, and A6. A trend for a reduction of TH IR was observed in nigral DA cells associated with significant reductions in TH IR in striatal DA nerve terminals. Finally, increases in 5-HT and substance P (SP) IR were found in the nerve terminals of the substantia gelatinosa of the cervical spinal cord in the stress group. In the present experimental model evidence has been obtained for a maintained activation of the hypothalamic-pituitary-adrenal axis as evaluated 7 days after cessation of severe chronic immobilization stress. The reduction of 5-HT IR in various 5-HT cell groups indicates a reduction of 5-HT synthesis, which may also be associated with reduced 5-HT release from the nerve terminals, since no depletion was observed in terminal regions and in one case an increase in 5-HT IR was noted (substantia gelatinosa).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Chronic immobilization stress: evidence for decreases of 5-hydroxy-tryptamine immunoreactivity and for increases of glucocorticoid receptor immunoreactivity in various brain regions of the male rat. 276 Jun 6

This study examined several in vivo and in vitro factors which influence the release of [Met5]-enkephalin (Met-ENK) from male rat hypothalamic slices superfused in vitro. Met-ENK release was significantly stimulated by corticotropin-releasing hormone (CRH; 10(-12)-10(-8) M), an effect which was abolished in the presence of the CRH-receptor antagonist, alpha-helical CRF9-41 (10(-6) M). The amount of Met-ENK release diminished with time in experiments in which the slices were continuously exposed to CRH. The opioid receptor antagonist naloxone (10(-6) M) stimulated Met-ENK release, even in the presence of the Na+ -channel blocker tetrodotoxin (10(-6) M), a result indicating presynaptic opioid feedback inhibition of Met-ENK release. The role of gonadal steroids in the control of Met-ENK release in vitro was also examined. It was found that the basal and CRH-induced release of Met-ENK was not changed 1 week after castration. However, a significant increase in the basal release of this peptide was observed 4 weeks after gonadectomy, and the Met-ENK-releasing efficacy of CRH was found to be reduced. The Met-ENK content of hypothalami from 1-week castrates was not significantly changed from control levels, but was significantly reduced in those from 4-week castrates. These long-term effects of castration could be overcome by the subcutaneous implantation of testosterone-containing capsules at the time of castration.
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PMID:Multiple factors influencing the in vitro release of [Met5]-enkephalin from rat hypothalamic slices. 278 52

Recombinant human interleukin-1 beta (IL-1 beta) significantly increased prostaglandin E2 (PGE2) in a dose-dependent manner in rat astrocyte culture. The minimum effective dose of IL-1 beta was 10(-10)M. IL-1 alpha also increased PGE2, but at a higher concentration. The minimum effective dose of IL-1 alpha was 10(-8)M, indicating it to be 100-fold less effective than IL-1 beta. On the other hand neither IL-1 beta nor IL-1 alpha increased PGE2 production by neuron cultures at any concentration tested. PGE2 response to IL-1 beta was suppressed by simultaneous addition of CRH, somatostatin-14 and LHRH, while these neuropeptides alone did not alter the basal PGE2 levels. Substance P, vasoactive intestinal polypeptide and alpha-MSH altered neither basal nor IL-1 beta-induced increase in PGE2 levels. Angiotensin II (AII) alone also increased PGE2 in cultured astrocytes. Combined addition of AII and IL-1 beta induced a synergistic effect in increasing PGE2 levels. The direct action of IL-1 beta on astrocyte culture suggests that astrocytes may be the target cells for IL-1 beta in the central nervous system. In view of the essential role of central PGE2 in IL-1 beta-induced CRH/ACTH release, these findings suggest the presence of a sophisticated regulatory network in the immune-neuroendocrine interaction.
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PMID:Interleukin-1 beta increases prostaglandin E2 in rat astrocyte cultures: modulatory effect of neuropeptides. 278 13

It has been suggested that limbic system-hypothalamic "overdrive" may be the underlying mechanism causing an augmented secretion of corticotropin releasing hormone (CRH), heightened adrenocortical responsiveness to corticotropin (adrenocorticotropic hormone) (ACTH), and alteration in cortisol feedback regulatory mechanisms as demonstrated by the dexamethasone suppression test. We examined pituitary and adrenocortical responses after morning administration of ovine CRH (oCRH) in 26 depressed patients and 11 healthy volunteers. Basal plasma ACTH concentrations were similar in both groups, whereas patients had a significantly diminished cumulative ACTH response after administration of oCRH. In contrast, basal total cortisol concentrations and cumulative cortisol responses to oCRH were similar in depressed patients and controls. Patients with melancholic features demonstrated the most profound ACTH blunting after oCRH, whereas patients separated according to dexamethasone suppression test results had similar ACTH and cortisol responses to oCRH. The present results extend data from prior studies utilizing oCRH in the evening and demonstrate a dysregulation of the functional integrity of the hypothalamic-pituitary-adrenocortical axis in depressive illness after a morning oCRH test at both central and peripheral hypothalamic-pituitary-adrenocortical axis sites.
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PMID:Pituitary and adrenocortical responses to the ovine corticotropin releasing hormone in depressed patients and healthy volunteers. 282 Mar 40

The effects of low doses (0.03 and 0.1 microgram/kg) of ovine CRH (oCRH) on plasma beta-endorphin/beta-lipotropin (beta End/beta LPH), ACTH, and corticosteroid levels were studied in normal men. The 0.03 microgram/kg oCRH dose produced a reproducible response, with a rapid increase in plasma oCRH to peak levels between 45 and 95 fmol/mL and an appropriate doubling of plasma peptide and corticosteroid concentrations. The relationship between the corticosteroid rise and the rapid beta End/beta LPH and ACTH declines suggested negative feedback by corticosteroids on the release of these pituitary products. Plasma oCRH levels were proportionate to those reported in studies using much higher oCRH doses, and produced plasma oCRH levels in the reported range for the hypophyseal portal circulation. Molecular sieving of the beta End-immunoreactive materials in basal and post-oCRH (0.1 microgram/kg) plasma samples revealed an average basal beta End to beta LPH ratio of 1:1.5; 15 min after oCRH stimulation the average ratio was 4:1. We conclude that a low (threshold) dose of oCRH can reliably stimulate POMC peptide secretion and may preferentially release beta End from the anterior pituitary.
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PMID:Effects of low dose ovine corticotropin-releasing hormone in humans: endocrine relationships and beta-endorphin/beta-lipotropin responses. 282 22

The existence of feedback inhibition of ACTH on its own secretion has been postulated. To investigate its existence in man, the effects of synthetic ACTH 1-24 on endogenous ACTH secretion were tested in 13 patients with Addison's disease. Plasma ACTH was measured using an immunoradiometric assay, specific for endogenous ACTH 1-39. Ten patients were given 50 micrograms ACTH 1-24 as a bolus iv dose followed by a 50-microgram infusion in 90 min. Blood samples for ACTH and cortisol assay were obtained at 0, 15, 30, 60, 90, and 120 min. As a control, a saline infusion was given 2 days earlier. Three other patients were given 100 micrograms ovine corticotropin-releasing hormone (oCRH) iv and ACTH 1-24 as described above. Blood samples for ACTH and cortisol assay were drawn every 15 min for 2 hours. A CRH test was performed during saline infusion as a control 2 days earlier. In all patients steroid replacement therapy was maintained during the studies. ACTH 1-24 caused a significant decrease (P less than 0.01) in endogenous plasma ACTH at 15 min compared to saline. oCHR administration markedly stimulated ACTH release in the three patients tested, and the ACTH response to oCRH was completely inhibited by the simultaneous administration of ACTH 1-24. These findings strongly support the presence of ACTH autoregulation in man. The complete inhibition of the ACTH response to oCRH by exogenous ACTH 1-24 provides evidence for ultra-short feed-back inhibition at the pituitary level.
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PMID:Evidence for ultra-short loop autoregulation of adrenocorticotropin secretion in man. 282 4

In this report, a case of Cushing's syndrome due to primary multinodular corticotrope hyperplasia is described. The patient had typical features of Cushing's syndrome and dynamic pituitary-adrenal testing, which suggested an ectopic adrenocorticotropic hormone (ACTH) syndrome. Results of petrosal sinus catheterization indicated that the pituitary gland was the source of excess ACTH. Total hypophysectomy resulted in complete remission of Cushing's syndrome. Light microscopic and immunohistochemical studies revealed multinodular corticotrope hyperplasia. Plasma corticotropin releasing hormone (CRH) was undetectable, and computed tomography of the chest and abdomen disclosed no neoplastic source of CRH. We speculate that either an abnormality in hypothalamic CRH secretion or corticotrope hypersensitivity to CRH might have been responsible for Cushing's syndrome in this patient.
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PMID:Cushing's syndrome due to primary multinodular corticotrope hyperplasia. 283 Apr 41

There is evidence that the peptides derived from proopiomelanocortin as well as the neurohypophyseal hormones exert important and substantial effects on brain functions after intracerebroventricular and peripheral administration. This led us to study the effects of intravenous hCRH on brain functions in humans using electroencephalographic techniques. In our experience the event-related potentials (e.g. auditory evoked potentials) provide a sensitive and accurate assay systems to study such effects of peptides. Male volunteers were tested in a dichotic listening paradigm, providing electrophysiological measures of selective attention. Human CRH (50 micrograms/hr i.v.) augmented selective attention as indicated by an increased difference between evoked potential waveforms to attended and to unattended stimuli. The opposite results, a decrease in selective attention, was observed after treatment with the behavioral active fragment of adrenocorticotropin, ACTH 4-10. In comparison to ACTH 4-10, lysine-vasopressin, and cortisol, CRH displayed a unique pattern of influences on event related potentials. From these results we conclude that CRH can affect brain function in man and does so by a direct action on the brain and not only by stimulating the release of other behavioral active hormones.
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PMID:Effects of corticotropin releasing hormone on human brain function: an analysis based on auditory evoked potentials. 283 98


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