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)

Hemodialysis resulted in remission of psychopathological symptoms in eight of ten chronic schizophrenics and successful hemodialysis was associated with a decrease of leucine endorphin levels in the blood. Three endorphins (endogenous peptides) have been isolated from the brain, and among them beta-endorphin was found to be the most potent in inducing behavioral changes in the rat. Nevertheless, neither a positive, nor an inverse relationship between the severity of schizophrenic psychopathology and CSF endorphin concentrations could be borne out by clinical experiments. Most recently, on the basis of an entirely different line of research, the possibility that schizophrenia is a prostaglandin deficiency disease has been raised.
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PMID:Some recent biochemical findings with possible therapeutic implications for schizophrenia. 20 79

With the discovery of the opiate peptides, several major avenues of research became apparent. These peptides produced a great deal of focused attention on their anatomy, biochemistry, and physiology. In this article, we present an overview of some of the main research issues and recent findings in the field of opiate peptides. The possible relationship of the opiate peptide neuronal systems to schizophrenia is discussed in light of attempts to alter schizophrenic symptoms with opiate antagonists, beta-endorphin, and dialysis. It is hypothesized that if the opiate peptides are involved in schizophrenia, then their involvement with dopamine systems and/or with stress responses may be critical.
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PMID:Some observations on the opiate peptides and schizophrenia. 21 30

Measurements of beta-endorphin-like immunoreactivity have been performed in CSF and plasma of patients with schizophrenia and other neuropsychiatric disorders. The detection limit of the RIA was between 20--50 pg/ml (6--15 fmole/ml). In CSF the quantity of beta-endorphin-like immunoreactivity ranges up to 65 pg/ml. The data from schizophrenics and other neuropsychiatric patients show no obvious deviation from the results in a control group of medical patients with normal CSF findings. In plasma the immunoreactive beta-endorphin-like material ranges up to 250 pg/ml. There is only a small tendency to higher values in schizophrenic patients, if compared with different types of neuroses and affective and organic psychoses. In a second series of experiments also this tendency could not be reproduced. In 9 electroconvulsive treatments an increase of blood beta-endorphin-like immunoreactivity was observed 7 times. A possible endorphinergic mechanism in the mode of action of electroconvulsion is hypothesized.
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PMID:beta-Endorphin-like immunoreactivity in cerebrospinal fluid and plasma of patients with schizophrenia and other neuropsychiatric disorders. 48 50

Beta-Leu5-endorphin, a relative of "normal" beta-endorphin in which leucine is substituted for methionine at position 5 of the latter, has previously been found in high concentrations in the dialysate of schizophrenics. Its removal from plasma by means of hemodialysis has been claimed to relive the symptoms of schizophrenia. Using a highly sensitive radioimmunoassay of equal sensitivity to beta-endorphin and beta-leu5-endorphin, we have compared the plasma immunoreactivity of three schizophrenic patients befofe and after performance of their first session of membrane hemoperfusion. As compared to normal subjects, plasma beta-endorphin-like immunoreactivity was not greatly elevated in the schizophrenic patients before hemoperfusion.However, instead of the expected decrease, a consistent increase in the plasma levels of immunoreactive beta-endorphin was detected after hemoperfusion. In vitro experiments in which two different membranes and hemodialysis as well as hemoperfusion were used, revealed that synthetic beta-leu5-endorphin (and beta-endorphin) from human plasma was not cleared with any of these methods. This finding is inconsistent with the hypothesis that the claimed therapeutic effects of hemodialysis in schizophrenics are due to the removal of a beta-endorphin-like material from the plasma. Consequently, it seems to be unprobable that high concentrations of beta-leu5-endorphin occur in the dialysate or ultrafiltrate of schizophrenics.
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PMID:Endorphins in schizophrenia: hemodialysis/hemoperfusion are ineffective in clearing beta-Leu5-endorphin and beta-endorphin from human plasma. 53 84

Some investigators have speculated that structural brain alterations observed in some psychiatric patients might be related to increased limbic-hypothalamic-pituitary-adrenal axis (LHPA) activity. To explore this hypothesis, we prospectively studied 166 research volunteers (19 patients with research diagnostic criteria (RDC) major depression, 9 patients with RDC bipolar depression, 45 patients with RDC schizophrenia, and 94 RDC normal controls), examining the relationship between magnetic resonance image-determined ventricular-to-brain ratio (VBR) and indices of LHPA axis function (cerebrospinal fluid (CSF) corticotropin-releasing factor (CRF), CSF adrenocorticotropic hormone (ACTH), and 24-hour urinary-free cortisol secretion). We observed no significant differences in mean VBR among the three patient groups and the normal control volunteers. Of the indices of LHPA activity, only CSF CRF concentrations distinguished the four subject groups, with CSF CRF being significantly elevated in the more severely depressed major depression patients. Indices of LHPA activity were not significantly correlated with VBR in any of the three patient groups or in the normal volunteers. These preliminary results suggest that VBR is not highly associated with alterations in LHPA activity, at least as determined cross-sectionally. Further longitudinal studies with reference to diagnostic subtypes, severity, symptom profiles, and more specific neuroanatomic regions may allow the elucidation of possible relationships between LHPA pathology and structural brain alterations.
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PMID:Limbic-hypothalamic-pituitary-adrenal axis activity and ventricular-to-brain ratio studies in affective illness and schizophrenia. 131 68

Cerebrospinal-fluid (CSF) corticotropin-releasing hormone, somatostatin, and thyrotropin-releasing hormone were measured by specific radioimmunoassays in 257 hospitalized psychiatry patients suffering from dementia disorders (n = 85), schizophrenia (n = 104), and mood and anxiety disorders (n = 39). Neurological controls (n = 29) were also investigated. Since there were large overlaps of the peptide levels across the nosological groups we subjected the dataset to a three-dimensional normal mixture distribution analysis. We obtained four biochemically separable clusters. Dementia disorders, but not the others, were heterogeneously distributed in these clusters but after eliminating the effects of age and illness duration this difference disappeared. No single clinical, psychological, or background variable emerged as a prominent correlate of the neuropeptide clusters. It is concluded that although CSF neuropeptide concentrations in psychiatric patient populations appear to be separable into distinct, normally distributed subgroups this distinction does not coincide with present nosological classifications.
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PMID:Cerebrospinal-fluid neuropeptides: a biochemical subgrouping approach. 136 69

The possibility of an involvement of peptidergic systems in schizophrenia has been under investigation for a number of years. Studies of the efficacy of des-tyr-gamma-endorphin were equivocal; more recent studies with des-enkephalin-gamma-endorphin have reported some activity but the peptide has only been investigated as an adjunct to neuroleptic medication, apart from one very small active reference comparator study. In the multicentre study reported here, 96 patients suffering from schizophrenia (DSM-III with a current exacerbation if chronic) were allocated randomly to double-blind treatment with either des-enkephalin-gamma-endorphin (DE-gamma-E) (Org 5878) 10 mg given as a once daily intramuscular injection for 4 weeks, thioridazine 400 mg orally in 2 divided doses or placebo using a double-dummy technique to preserve blindness. There was a significant advantage for thioridazine compared with placebo registered on all measures at weeks 3 and 4. There was no difference between DE-gamma-E and placebo. There was a significant difference between thioridazine and DE-gamma-E at weeks 3 and 4 registered on the MSS and at week 3 registered on the BPRS. The lack of efficacy of DE-gamma-E suggests that the theories that the endorphins have an important role in schizophrenia have to be revised. The need for well designed placebo controlled studies for assessing efficacy in schizophrenia is emphasized.
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PMID:Inadequate treatment response to des-enkephalin-gamma-endorphin compared with thioridazine and placebo in schizophrenia. 152 45

Complementary oligonucleotide probes specific for the human pro-opiomelanocortin (POMC) mRNA were used to analyze the expression of POMC gene in 56 human postmortem pituitaries by in situ hybridization histochemistry. POMC transcripts were visualized by autoradiography in anterior lobe of the pituitary where their distribution was in a 'patchy-like' pattern. No hybridization could be observed in the posterior lobe of the pituitary. We examined pituitaries from several controls and from patients dying with schizophrenia, Parkinson's disease. Alzheimer's disease, Wernicke's encephalopathy and depressive illness. Computer-assisted microdensitometric semiquantification of POMC mRNA using a complementary oligonucleotide as hybridization standard, revealed no statistically significant effect of postmortem delay (between 2.5 and 66 h), of gender, age (between 22 and 103) or cause of death in 56 human pituitary glands. A large variation in POMC levels was already observed among all 30 control cases. The levels of POMC mRNA observed in pituitaries from different pathologies did not show a significant variation when compared with control cases.
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PMID:Study of pro-opiomelanocortin mRNA expression in human postmortem pituitaries. 171 87

Plasma levels of prolactin, growth hormone, corticotropin, and cortisol were measured at 15-minute intervals for 24 hours in nine unmedicated male schizophrenic patients and in nine age-matched normal male subjects. Each study was preceded by 3 days of habituation to the laboratory environment. Sleep was polygraphically recorded. The circadian and pulsatile variations present in each hormonal profile were quantitatively characterized with the use of computer algorithms specifically designed for analyses of hormonal fluctuations. The major abnormality of neuroendocrine release that was observed in the schizophrenic patients was an almost threefold enhancement of the sleep-related increase in the prolactin level, associated with an intensified frequency of nocturnal prolactin pulses. This increased stimulatory effect of sleep on prolactin secretion was evident immediately after sleep onset. The normal inhibition of cortisol secretion during early sleep was absent in schizophrenic patients. The major sleep abnormalities were a prolonged sleep latency and a reduction in total rapid eye movement stage sleep. During wakefulness, prolactin and cortisol levels were normal. The 24-hour profile of growth hormone was unaltered in schizophrenic patients, and a sleep-onset growth hormone pulse was observed in all patients. No abnormalities were noted in the levels or temporal organization of corticotropin secretion. Both the amplitude and the timing of the cortisol rhythm were normal. We conclude that, in schizophrenic men, pituitary-adrenal function and circadian time-keeping are normal but prolactin secretion is hyperresponsive to the physiologic stimulus of sleep onset. Schizophrenia thus appears to be characterized by a subset of neuroendocrine disturbances distinct from that observed in major endogenous depression.
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PMID:Circadian and sleep-related endocrine rhythms in schizophrenia. 184 71

In seventy-two patients affected by hyperphagic obesity and forty age-matched, normal weight volunteers we performed a psychological assessment, through various mental tests, and evaluated the beta-endorphin (B-Ep), ACTH and cortisol circulating levels, in basal condition and following an overnight short dexamethasone suppression test (DST). The hormones were measured by radioimmunoassay either directly in the serum (cortisol) and the plasma (ACTH), or after affinity gel column chromatography (B-Ep). In obese subjects B-Ep levels in basal conditions were four times greater than in normal weight controls and showed significantly less reduction after DST. ACTH and cortisol levels, in contrast, were in the normal range and were suppressed following dexamethasone as was also true in the control group. Psychological evaluation on M.M.P.I. (Minnesota Multiphasic Personality Inventory) revealed a trend toward hypochondria, depression, hysterias, psychoasthenia and schizophrenia. However, no significant correlation has been found between M.M.P.I. clinical scale scores and circulating levels of B-Ep and cortisol either in basal conditions or after DST. In conclusion, these data do not support the hypothesis that abnormalities of the hypothalamus-pituitary-adrenal axis in hyperphagic obesity are related to affective disorders.
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PMID:Hyperendorphinemia in obesity is not related to the affective state. 196 3


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