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

The etiology of the SAS is unknown. To test whether endogenous opioids could be pathologically active in SAS, markers of opioid systems were measured in the CSF of 15 patients with SAS and in control subjects. Measured by receptor assay, the concentration of so-called fraction 1 opioid was higher in patients with SAS (3.0 +/- 1.5 pmol/ml; mean +/- SD) than in control subjects (1.1 +/- 0.5 pmol/ml) (p less than 0.01), whereas that of fraction 2 opioid was similar in the two groups. Beta-endorphin-like activity, measured by radioimmunoassay, was somewhat lower in patients with SAS (14.0 +/- 2.8 pmol/ml) than in control subjects (21.8 +/- 7.6 pmol/ml) (p less than 0.05). Six months after surgical treatment of the soft palate, new measurements were made in eight patients. Fraction 2 endorphin and beta-endorphin showed no consistent changes. A decrease in the level of fraction 1 from 4.1 +/- 1.5 pmol/ml to 2.3 +/- 1.0 pmol/ml (p less than 0.02) was noted in those six patients showing a successful clinical course. The data support the hypothesis that in SAS the opioid activity is increased.
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PMID:Increased CSF opioid activity in sleep apnea syndrome. Regression after successful treatment. 252 20

Endogenous opioid systems may be altered as a consequence of addiction, but evidence to support this idea is meager so far. We obtained 136 cerebrospinal fluid (CSF) samples from 72 opioid addicts during four distinct states: methadone maintenance, detoxification from methadone, opioid antagonist treatment, and drug-free status. CSF endorphins were measured in 86 patients samples using a radioreceptor assay (RRA), and beta-endorphin levels were measured in 85 patient samples using a radioimmuno assay (RIA). During detoxification, both RRA fraction I and beta-endorphin showed a generally similar pattern of changes. Both were lowest when measured 40-50 hr after the last opioid dose, and both showed an apparent rebound to higher than methadone maintenance values at 60-70 hr following the last dose. During methadone maintenance and drug-free states, the addicts' levels of fraction I RRA endorphins in the CSF were higher than levels found in a normal control group. Fraction II endorphins were also elevated in the addicts who were drug free. In contrast, CSF beta-endorphin during both methadone maintenance and drug-free states was lower in the addicts as compared to the normal, drug-naive group. Except for the pattern found during detoxification, there were no consistent changes in endorphin levels across different states of addiction.
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PMID:Endogenous opioids in cerebrospinal fluid of opioid-dependent humans. 284 15

The present study was conducted to examine roles of brain monoamines and opioid peptides in growth hormone (GH) secretion in unanesthetized, freely behaving rats. The administration of chlorpromazine (CPZ, 300 microgram/100 g, i.v.), an antagonist of brain monoamines, to rats that were passively immunized with antiserum to somatostatin immediately lowered plasma GH levels and inhibited episodic GH secretion. An intraventricular injection of beta-endorphin (3.5 microgram) stimulated GH secretion. This effect was completely inhibited by the prior administration of naloxone (100 microgram/100 g, i.v.), a specific antagonist of opioid peptides, but not by CPZ. In addition, the administration of naloxone did not inhibit episodic GH secretion. The results suggest that CPZ inhibits episodic GH secretion via a factor(s) other than somatostatin. It is also inferred that brain monoamines, but not opioid peptides, play major roles in the regulation of episodic GH secretion in rats.
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PMID:Effects of chlorpromazine and naloxone on growth hormone secretion in rats. 610 6

Three hundred cases were treated by AES in an out-patient detoxification setting. Seventy-seven cases completed 14 days of treatment and of these 30 were detoxified. One hundred and twenty-six cases came back for retreatment and another 19 cases (19/300 = 6.3% or 19/126 = 15.5%) were detoxified. It was found that the ACTH, cortisol (corticosterone), c-AMP were elevated during abstinence and these compounds were reduced after AES treatment. Fraction I of the opiate activity in the brains of mice was found to be increased after AES. It has been suggested that this could be a beta-endorphin. Recently it was found that during abstinence the plasma beta-lipoprotein and and beta-endorphin were elevated but not reduced after AES. However, the CSF met-enkephalin was within normal limits during abstinence but greatly elevated after half an hour of AES. It is suggested that acupuncture affects not only the somatosensory nervous system but also the autonomic nervous system, as well as the neuro-endocrine system in drug abusers.
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PMID:Clinical experience and mechanism of acupuncture and electrical stimulation (AES) in the treatment of drug abuse. 611 57

The effects of beta-endorphin, MIF-I, and alpha-MSH on d-amphetamine- a CPZ-induced hypothermias in rats kept at 4 degrees C were tested in three experimental groups: (a) intact; (b) rats with lesions of the olfactory tubercle; and (c) rats in which the link between the DA mesolimbic pathway and the striatum was disconnected. All drugs tested alone (except MIF-I) caused significant hypothermia. Pretreatment with CPZ, MIF-I, and alpha-MSH potentiated d-amphetamine-induced hypothermia in intact rats. Pretreatment with alpha-MSH potentiated CPZ-induced hypothermia. beta-Endorphin partially blocked d-amphetamine-induced hypothermia, but did not interact with CPZ, MIF-I, or alpha-MSH. All potentiations were either reduced or disappeared in the incisioned rats. CPZ and alpha-MSH caused hypothermia in olfactory tubercle-lesioned rats. The results indicate that: (a) the DA mesolimbic pathway is involved in the hypothermic response of all drugs tested; (b) an intact feedback loop is required for the potentiation of the hypothermic response of CPZ on d-amphetamine, MIF-I on d-amphetamine, and alpha-MSH on d-amphetamine and CPZ; (c) beta-endorphin acts as a partial blocker of d-amphetamine; MIF-I is a weak potentiator of d-amphetamine, alpha-MSH acts as a negative modulator of the DA system, most probably in the striatum.
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PMID:Modification of d-amphetamine- or chlorpromazine-induced hypothermia by beta-endorphin, MIF-I, and alpha-MSH: mediation by the dopaminergic system. 612 51

Opioid peptides have been purified from large pooled samples of human cerebrospinal fluid. The purification steps involved chromatography on Sephadex G-10 and electrophoresis in agarose suspension. The purified material was further characterized by HPLC and radioimmunoassay. All procedures were guided by a specific radioreceptor assay. The Sephadex G10 fractionation yielded receptor activity in two discrete fractions, Fraction I (FI) and Fraction II (FII). A second Sephadex run of FII gave a partial resolution of two components, one of which was larger (FIIA). Electrophoresis resolved these fractions into several components, most of which showed a more basic behaviour than the enkephalins. Thus, FI separated into at least 4 components and FIIB into two components while FIIA remained a single peak. These components appeared to migrate as distinct peaks and some of them also chromatographed on a HPLC-column as single components. Considering their behaviour in electrophoresis and on HPLC, two components are suggested to represent known endorphin structures. The predominant FII component (FIIA) was thus indistinguishable from Met-enkephalin-Lys6 in all chromatographic systems and one of the most basic FI components showed close similarity with dynorphin. Each of these components occurs at a higher concentration than Met- or Leu-enkephalin, dynorphin or beta-endorphin.
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PMID:Characterization of electrophoretically separable endorphins in human CSF. 613 Aug 23

A 41-residue peptide purified as a corticotropin-releasing factor/beta-endorphin-releasing factor (CRF) in vitro was tested for its ability to stimulate the secretion of ACTH, beta-endorphin, and corticosterone in three animal groups: 1) unanesthesized rats bearing indwelling venous cannulae, 2) rats pretreated with chloropromazine plus morphine sulfate plus pentobarbital (CPZ-MS-Nb, and 3) rats with hypothalamic deafferentiations in the frontal and lateral retrochiasmatic areas. In all three bioassays iv administration of 0.1-10 micrograms CRF elicited a dose-related increase in plasma ACTH and beta-endorphin values over a 5- to 15-min period. Corticosterone secretion was also elevated but responded maximally with all doses of CRF tested. Pretreatment of CPZ-MS-Nb animals with 20 micrograms dexamethasone 4 h before assay abolished the CRF-induced hormone secretion. These data suggest that CRF may play a physiological role in the regulation of the hypothalamic-pituitary-adrenal axis.
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PMID:In vivo corticotropin-releasing factor-induced secretion of adrenocorticotropin, beta-endorphin, and corticosterone. 627 23

Using the spinal superfusion procedure, in anesthetized rats and cats, the presence of active factors which displace dihydromorphine in brain opiate binding studies, has been observed. Separation of this activity on a Sephadex G-10 column reveals the presence of two fractions which occur before (Fraction I) and after (Fraction II) the salt peak which account for over 70% of the observed dihydromorphine-displacing activity. The ratio of activity in Fraction II/Fraction I is 33 and 21, in the resting spinal perfusates of the rat and cat, respectively. High intensity, bilateral stimulation of the sciatic nerve in cats, results in a 30- and 5.4-fold increase in the levels of Fraction I and Fraction II, respectively, over pre-stimulation levels. In rat, bilateral stimulation of the hind paws, resulted in a frequency-dependent increase in the levels of Fraction I (1.9- and 3.2-fold at 5 and 50 Hz, respectively). Dynorphin 1-13 fragment elutes at least partly in Fraction I. With regard to Fraction II, the peak co-chromatographs with hexapeptide derivatives of enkephalin. Met- and Leu-enkephalin (Fraction III), elute off the column at a point where opiate receptor displacing activity is relatively small. Electrophoretic separation of Fraction I radioreceptor activity of alkaline and acid pH on agarose columns revealed two principle peaks which co-migrated with alpha-neoendorphin and dynorphin 1-13. Fraction II activity appeared primarily in a single peak which was isographic with enkephalin hexapeptides. Using radioimmunoassays, detectable levels of dynorphin and Met-enkephalin were observed and sciatic nerve stimulation resulted in significant increases. Neither column-coupled radioreceptor assays nor radioimmunoassays revealed the presence of beta-endorphin. The present experiments demonstrate the releasability by high intensity somatic stimulation of a variety of opioid peptides present in spinal terminals. Significantly, however, the majority of this activity appears to be found in fractions different from those of the pentapeptide enkephalins.
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PMID:Studies on the release by somatic stimulation from rat and cat spinal cord of active materials which displace dihydromorphine in an opiate-binding assay. 686 Sep 55

Basophil invasion, i.e., invasion of basophilic corticotrophs from the residual intermediate lobe into the posterior lobe of the human pituitary gland, is believed to be a physiological phenomenon. This study evaluated the distribution of CPE, CPD, CPZ, alpha-MSH, ACTH, and Ki-67 immunoreactivity between human anterior pituitary and basophil invasion of the neurohypophysis. Mild to moderate immunoreactivities for CPE and CPZ were distributed relatively uniformly in the majority of the anterior pituitary cells and basophil invasion. In contrast, only corticotrophs exhibited intense CPD immunoreactivity. Basophil invasion showed similar immunoreactivities for alpha-MSH, ACTH, CPE, and CPZ as corticotrophs in the anterior pituitary, except for CPD, which was detected much less frequently. In the posterior lobe, CPE, CPD, and CPZ were present within the Herring bodies. Although no MIB-1 immunoreactivity was identified in anterior pituitary cells, limited MIB-1 labeling was detected in basophil invasion in five of ten cases. Highly selective expression of CPD in corticotrophs suggests that CPD plays a particularly important role in prohormone (POMC) processing in corticotrophs, with minimal or no significant roles in non-corticotrophs. Evidence that corticotrophs in basophil invasion are undergoing proliferation and are also phenotypically different from their counterpart in the anterior pituitary has further raised the possibility of some neoplastic potential.
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PMID:Immunohistochemical localization and comparison of carboxypeptidases D, E, and Z, alpha-MSH, ACTH, and MIB-1 between human anterior and corticotroph cell "basophil invasion" of the posterior pituitary. 1137 25

The influence of pituitary adrenocorticotropic hormone (ACTH) and growth hormone (somatotropin, STH), singly and in combination, has been studied in normal, young adult rats, with respect to antibody formation against Fraction IA of Pasteurella pestis. When ACTH was administered during the period of immunization, in a daily dose just sufficient to prevent body weight increase relative to the non-treated, immunized controls, serum antibody levels against the specific antigen employed were significantly depressed. The administration of STH alone resulted in a marked increase in body weight. The increase in antibody level was not significant at the 5 per cent level when compared with the control values. The same dosage of STH given simultaneously with ACTH maintained body weight at a level slightly above that of the controls, and resulted in an effective counteraction of the antibody depression produced by the latter hormone.
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PMID:The influence of adrenocorticotropic and growth hormones on antibody formation. 1340 70


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