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)

beta-lipotrophin (beta-LPH) and beta-endorphin (beta-EP) plasma levels were measured by radioimmunoassay after glass powder extraction and Sephadex G-75 column chromatography in plasma samples from controls (ten healthy males and twenty-six young women in early follicular phase), from eighty-two pregnant women in weeks 9-40 after their last menstrual period, from nine women just after delivery and the cord blood of their neonates, in fifteen mixed cord blood samples and in seven amniotic fluid samples obtained by amniocentesis. No sex differences were found in beta-LPH (120.6 +/- 8.5 pg/ml) or beta-EP (31.1 +/- 2.4 pg/ml) plasma levels or in their molar ratio (1.34 +/- 0.09) (MR). beta-LPH plasma levels increased in early pregnancy (13-16 weeks) (185.0 +/- 27.1 pg/ml) and remained high until weeks 21-24, then declining to levels similar to those of controls. beta-EP plasma levels were significantly depressed in weeks 9-12 (20.7 +/- 5.3 pg/ml), subsequently increasing to a maximum at weeks 36-37 (42.7 +/- 6.8 pg/ml). beta-LPH/beta-EP molar ratio was about double normal in early pregnancy and decreased to normal in the second half. The present data indicate that beta-LPH and beta-EP present different patterns throughout pregnancy and that beta-EP levels increase progressively, reaching the highest concentrations at term. At delivery, both beta-LPH and beta-EP showed maximum values (beta-LPH: 230.2 +/- 20.4 pg/ml; beta-EP: 78.0 +/- 7.4 pg/ml) and a MR of 1.02 +/- 0.10 indicating that stressful situations, such as labour, stimulate a simultaneous rise in beta-LPH and beta-EP plasma levels. Cord blood specimens showed a wide range of values (beta-LPH:75-347 pg/ml; beta-EP: 16-287 pg/ml) with a MR of 1.21 +/- 0.14. Amniotic fluid samples obtained late in the third trimester of pregnancy were characterized by beta-LPH levels of 119.4 +/- 26.4 pg/ml and beta-EP levels of 29.6 +/- 7.5 pg/ml.
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PMID:beta-lipotrophin and beta-endorphin plasma levels during pregnancy. 626 4

Pro-opiocortin, the precursor of ACTH, LPH and gamma-MSH, is biosynthesized in both the cells of the pars intermedia and the corticotrophs of the pars distalis. In the pars distalis its processing does not vary significantly from species to species whereas in the pars intermedia large differences occur. The release of ACTH, beta-LPH and pro-gamma-MSH from the corticotrophs is under common positive control by hypothalamic corticotropin-releasing factor (CRF) and the nature of the peptides remains unchanged when they are secreted. The release of all five pars intermedia peptides that we have measured in vitro appears to be under tonic dopaminergic inhibition. The secreted peptides have also been identified chromatographically. The lack of unequivocal physiological function in the periphery, the diversity of the pars intermedia peptides and this common control mechanism tend to preclude a simple endocrine role for the pars intermedia. The neural effects of MSH and endorphin are well documented and specific neuronal uptake therefore cannot by dismissed. The absence of pars intermedia in the adult human pituitary suggests that such a site of synthesis of these peptides plays a minor role in learning and behaviour in a species (such as Homo sapiens) that has a highly evolved intelligence and may, instead, need to synthesize the peptides only in the brain.
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PMID:Nature and control of peptide release from the pars intermedia. 626 76

A combination of radioimmunoassays and chromatography under acid-dissociating conditions has been used to obtain profiles of ACTH and LPH-related peptides in human plasma and cerebrospinal fluid. The spectra of peptides observed in these two fluids differ markedly. ACTH, beta-LPH, gamma-LPH and beta-endorphin are observed in the plasma of normal subjects and patients with increased pituitary ACTH secretion, whereas cerebrospinal fluid contains ACTH, beta-LPH, gamma-LPH and beta-endorphin, a 31 000-molecular-weight putative precursor having ACTH, LPH and gamma-MSH immunoreactivities, as well as pro-gamma-MSH(1-77) and smaller immunoreactive gamma-MSH fragments, alpha-MSH was not observed in blood or cerebrospinal fluid but this pars intermedia peptide and corticotropin-like intermediate lobe peptide (CLIP) were both found in tumour tissues obtained from patients with the ectopic ACTH syndrome. In vitro studies of human pituitary tumour tissues confirmed concomitant secretion of ACTH, beta-LPH, gamma-LPH, beta-endorphin and pro-gamma-MSH, which could be stimulated by a preparation of crude stalk median eminence and synthetic arginine vasopressin, from the rat, and could be suppressed by hydrocortisone. Clinical studies in which electroacupuncture was used to alleviate the symptoms of heroin withdrawal or recurrent pain revealed that concentrations of met-enkephalin and beta-endorphin, respectively, may rise in cerebrospinal fluid in association with relief of symptoms.
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PMID:Pars intermedia peptides: studies in adult humans. 626 79

The immunologic patterns of 3 human pituitary adenomas of Cushing's disease have been studied after gel exclusion chromatography (Sephadex G-50). The immunologic characteristics were examined with three radioimmunoassays specific for human corticotropin (ACTH), lipotropin (LPH) and beta-endorphin (beta-End). In cell tumor extracts, chromatographic peaks corresponding to beta-LPH, gamma-LPH, beta-End and ACTH were identified. The ACTH/beta-LP-beta-End ratio was 1 in the 3 cases. Additionally, in the 3 cases, a chromatographic peak, partially cross-reacting in the beta-End assay, was eluted after beta-End, thus suggesting the presence of a fragment of the molecule. In 1 case, a peak of large molecular weight material with N- and C-terminal beta-LPH and ACTH immunoreactivity was observed, which corresponded to the precursor material. The release and the effects of various stimuli were studied on dispersed tumor cells in primary culture. The tumor cells had a biphasic basal secretion rate with a rapid increase of ACTH/beta-LPH-beta-End in the culture medium during the first 2 h. Then the release, studied during 2 days, was slower. Chromatographic studies showed that the beta-LPH/beta-End ratio was 0.8 in the cells and 0.3 in the medium, due essentially to the release of beta-End and beta-End-like materials. The cells released ACTH and beta-LPH-beta-End in equimolar ratio after stimulation with arginine vasopressin (AVP). The maximum effect was obtained with 10(-6) M AVP (D50 = 1 10(-9) M). Dibutyryl cyclic AMP (2. 10(-3) M) induced maximal release of ACTH/beta-LPH-beta-End. This stimulation was suppressed by a 48-hour preincubation with dexamethasone (10(-8)-10(-6) M). There was no effect of TRH and LH-RH on cell release. Dopamine (10(-6) M) specifically blocked the release of ACTH/beta-LPH-beta-End in 1 case. These data showed (a) heterogeneity of chromatographic profiles from case to case; (b) the presence of material in the tumor, cell extracts and culture medium corresponding to fragment(s) of beta-End; (c) culture studies demonstrated that tumor cells remain responsive to AVP stimulation and dexamethasone suppression, and (d) the dopamine inhibition of ACTH and beta-End release needs further investigation.
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PMID:[Lipocorticotropic peptides in Cushing's disease: in vitro studies]. 626 12

Studies in the experimental mouse pituitary tumor cell line AtT-20/D-16-v have recently shown that ACTH, the lipotropins (beta- and gamma-LPH), beta-endorphin (beta-End) and the 16-K fragment are synthesized through a common precursor molecule which is a 31,000 glycopeptide (pro-ACTH/endorphin). We have investigated whether such a biosynthetic model might exist in man. Radioimmunoassays have been developed against human ACTH, N-terminal LPH, beta-End or C-terminal beta-LPH, C-terminal gamma-LPH, and the 16-K fragment or N-terminal pro-ACTH/endorphin. These radioimmunoassays were used to examine various human samples before and after gel fractionation in ordinary or denaturing buffers. Medium DMS-79, in which human small cell carcinoma cells derived from a lung cancer were cultured, was shown to contain molecules identical to gamma-LPH, beta-LPH, beta-End and ACTH. In addition, it also contained a high molecular weight material with LPH, beta-End, and ACTH immunoreactivity. These three immunoreactivities could not be dissociated under denaturing conditions (6 M guanidine-HCl), and were all absorbed on an ACTH-purified anti-(1-24)-ACTH affinity column. Medium DMS-79 also contained high molecular weight calcitonin immunoreactivity that was not absorbed on the (1-24)-ACTH affinity column and therefore was not part of the pro-ACTH/endorphin molecule. Extracts from two pheochromocytomas responsible for the ectopic ACTH syndrome were found to contain, in addition to ACTH, large amounts of gamma-LPH and beta-End. High levels of beta-LPH and beta-End were also present in the plasma from a patient with the ectopic ACTH syndrome due to pancreatic carcinoma. Plasma immunoreactive 16-K fragment was increased in another patient with this syndrome. These results indicate that a biosynthetic model similar to that described in the AtT-20/D-16-v mouse tumor cell line also exists in man. Tumors responsible for the ectopic ACTH syndrome provide a unique source to study this model in man.
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PMID:[Ectopic secretion of ACTH and of related peptides (LPHs, beta-endorphin, "16K"). Evidence for a common precursor]. 626 15

Immunoreactive ACTH and beta-lipotropin (beta-LPH) plasma concentrations are elevated in clinically stable chronic renal failure patients on hemodialysis (LPH: patients, 271.8 +/- 35.7 fmol ml-1; normal subjects; 6.6 +/- 0.5; ACTH: patients, 56.4 +/- 15.3; normal subjects, 19.4 +/- 1.7). To begin to study the etiology of such elevated levels, the MCR, apparent volume of distribution, and fractional rate of disappearance of synthetic human ACTH and highly purified human beta-LPH were determined in two clinically stable chronic renal failure patients on hemodialysis, after bolus simultaneous injection of both peptides. Biphasic disappearance curves were obtained for beta-LPH; triphasic for ACTH. The MCR of ACTH was within the range seen in normal subjects, whereas the MCR of beta-LPH was less than one half the normal rate. The data indicate that a decrease in MCR (rather than an increase in pituitary secretory rate) may account for the higher plasma levels of beta-LPH in uremic patients.
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PMID:Impaired clearance of beta-lipotropin in uremia. 627 Jan 75

The distinctive chromatographic patterns of beta-endorphin-like immunoreactivity (beta END-LI) released from rat pars distalis (PD) or pars intermedia in vitro as well as the selective inhibitory effects of dexamethasone on PD were used to determine which lobe secretes beta END-LI into plasma after clonidine administration in vivo. Gel chromatography (Sephadex G-50) indicates that cultured PD cells released two major immunoreactive species which coelute with beta-lipotropin (beta LPH) or beta END standards. Conversely, virtually all of the beta END-LI secreted by neurointermediate lobe [pars intermedia plus pars nervosa (NIL)] cells in vitro resembled beta END in size, while none was detected which cochromatographed with beta LPH. Incubation of PD cells with clonidine (10(-6) M) evoked a 2-fold increase in beta END-LI release, while the drug had no effect on beta END-LI released from cultured NIL cells. Dexamethasone (10(-7) M) inhibited the clinidine-induced release of beta END-LI from PD cells, whereas it did not influence the stimulated release of beta END-LI from NIL by isoproterenol (10(-6) M). In vivo administration of clonidine (0.5 mg/kg, ip, for 15 min) increased total plasma beta END-LI from 0.75 +/- 0.16 to 1.35 +/- 0.18 ng/ml; 85% of this rise corresponded to beta LPH as determined by gel chromatography. Prior administration of dexamethasone (60 micrograms/kg, ip, for 4 h) completely prevented the clonidine-induced release of beta END-LI in vivo. These results demonstrate that clonidine probably acts selectively on the PD in vivo to release pituitary beta END-LI, and further, that PD can release beta END-LI independently of the pars intermedia.
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PMID:Evidence for independent secretion of beta-endorphin immunoreactivity from rat pars distalis in vivo. 627 37

Using RIAs for six regions within proopiolipomelanocortin (proOLMC), gel filtration, and electrophoresis, we studied pituitary peptides in a normal horse and one with Cushing's disease caused by a pars intermedia adenoma. Almost all immunoreactive (IR) ACTH (78%) was 4,500 mol wt (4.5K) ACTH in normal pars distalis, but it was almost 100% corticotropin-like intermediate lobe peptide (CLIP) in normal pars intermedia. alpha MSH and beta MSH were found mainly in pars intermedia: equal concentrations of the beta MSH precursors, beta-lipotropin (beta LPH) and gamma LPH, were found in pars distalis. Most IR-beta-endorphin (IR-beta END) was found as beta END in pars intermedia, but roughly equal concentrations of beta END and its precursor, beta LPH, were found in pars distalis. A 33K molecule containing IR-ACTH, IR-gamma 3MSH, and IR-beta END, presumed to be proOLMC, and a variety of 15-27K presumed biosynthetic intermediates were found in both normal pars distalis and pars intermedia. The pars intermedia adenoma causing Cushing's syndrome contained high IR-peptide concentrations. Several differences in precursors were noted, including the presence of three larger presumed precursors (38.5K, 47K, and 63K) that had both ACTH and beta END immunoreactivities and both deletions and additions of 15-27K intermediates. The Cushing's horse's plasma peptides reflected tumor concentrations; 4.5K ACTH was modestly elevated, but the concentrations of CLIP, alpha MSH, beta MSH, gamma LPH, and beta END were dramatically increased. About 20% of plasma IR-ACTH and 5% of IR-beta MSH and IR-beta END were found as high molecular weight forms. Normal processing of horse proOLMC appears to be similar to that in other species, but may be altered in pars intermedia tumors of horses with Cushing's disease, the plasma of which contains disproportionately increased concentrations of pars intermedia proOLMC peptides.
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PMID:Proopiolipomelanocortin peptides in normal pituitary, pituitary tumor, and plasma of normal and Cushing's horses. 627 64

Placental peptides, such as human chorionic gonadotropin (hCG) and human placental lactogen (hPL), which have marked homologies to pituitary peptides, were described in the early part of this century. Recently, the presence in placenta of additional peptides previously demonstrated as occurring in other tissues, such as brain and pituitary, has been reported. Their presence in placenta has been attributed to similar embryological origin of the tissues which share these peptides, although this has by no means been proven. Placental concentrations of these recently described peptides are several orders of magnitude lower than described for their original sites of production. In many instances, definitive characterization of structural identity with their extraplacental counterparts has not been performed, but has been based on indirect evidence obtained by immunoassay or immunocytochemistry. Evidence of placental synthesis has been obtained for hCG, hPL, and pro-opiomelanocortin (the precursor molecule for adrenocorticotropic hormone (ACTH), B-lipotropin (B-LPH), alpha-melanocyte-stimulating hormone (alpha-MSH), beta-endorphin, and other thus far uncharacterized peptides). Possible functions for the recently described peptides might include actions on the maternal or fetal systems or local (paracrine) actins affecting other placental constituents, although to date no definitive physiological roles have been demonstrated.
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PMID:Placenta as a source of 'brain' and 'pituitary' hormones. 627 87

6 healthy pregnant women, monitored with external cardiotocography, were studied. Blood samples were collected hourly throughout labour until delivery of the fetus and placenta, and again on the 5th day of puerperium. beta-Lipotropin (beta LPH) and beta-endorphin (beta EP) were determined by specific radioimmunoassays in each sample, after silicic acid plasma extraction and G-75 column chromatography. Both opioid plasma levels rise progressively during labour, reaching their highest values 1 h before delivery (beta LPH: 296.0 +/- 60.2 pg/ml; beta EP 106.2 +/- 40.6 pg/ml) as compared with values of 157.0 +/- 35.4 (beta LPH) and 57.0 +/- 7.3 pg/ml (beta EP) (mean +/- SE) at the beginning of labour. With the exception of 1 case, a significant correlation was observed between beta LPH and beta EP plasma levels. The two opioid plasma levels decrease after delivery of the placenta (272.5 +/- 59.6 and 118.2 +/- 68.4 pg/ml) and subsequently decrease further to levels of 105.6 +/- 46.4 (beta LPH) and 33.7 +/- 16.5 (beta RP) on the 5th day of puerperium. beta LPH and beta EP plasma levels showed a significant correlation throughout labour with the 'uterine contractility force/hour', which was calculated by the addition of tocographic areas of each uterine contraction at 1-hour intervals. These data demonstrate that the increase in plasma opioid concentrations during labor is directly related to the number and intensity of uterine contractions.
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PMID:Opioid plasma levels during labour. 628 96


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