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)

To investigate the role of endogenous opioid peptides in the pathophysiology of cerebral ischaemia, the CSF levels of immunoreactive beta-endorphin and leu-enkephalin in 16 patients with cerebral infarction were measured. Both the CSF beta-endorphin and leu-enkephalin levels in the acute stage of cerebral infarction were significantly higher than the values in the chronic stage. The CSF concentrations of the two peptides revealed a positive correlation in the acute but not the chronic stage. The increased endogenous opioid peptides in the CSF in the acute stage may modify the evolution of cerebral infarction.
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PMID:CSF beta-endorphin and leu-enkephalin levels in the acute and chronic stages of cerebral infarction. 295 70

"Reinforcing" effects are ascribed to endogenous opioids, particularly to the pro-opiomelanocortin (POMC)-derived beta-endorphin 1-31, the most potent opiate-active substance. Alcohol induces variations in the genetic processing of the precursor POMC and of beta-endorphin at different levels. Studies focused on changes in POMC gene expression (mRNA quantitation) and post-translational processing. Chronic alcohol intake significantly reduces POMC mRNA in the lobes of the pituitary. In inbred strains of mice, genotypic differences are seen in post-translational processing of hypothalamic beta-endorphin, thus inducing differences in alcohol sensitivity. Clinical studies show a disproportion of POMC cleavage products in the CSF of chronic alcoholics (reduced beta-endorphin versus increased ACTH contents), together with remarkable indications for baseline differences in beta-endorphin levels. Errors within the genetic sequence of POMC are suggested to underlie alcohol-seeking behavior.
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PMID:Beta-endorphin genetics in the etiology of alcoholism. 296 50

Methionine-enkephalin (ME-IR) and beta-endorphin (BE-IR) immunoreactive material CSF concentrations have been measured in subjects of different ages affected by lumbar or cervical disk hernia. The two peptides exhibited different age-related trends. ME-IR levels rose significantly with age while no changes were observed in the case of BE-IR.
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PMID:Age-related changes of methionine-enkephalin and beta-endorphin/beta-lipotropin immunoreactivity in human CSF. 297 45

Thyroliberin produces a marked depressant action on the reflex cerebrovascular constriction reactions. The lack of changes in the content of immunoreactive beta-endorphine in blood and CSF indicates that apparently the cerebrovascular effects of the drug are not mediated via the opioid system but are due to a direct influence of thyroliberin on the central mechanisms by which brain circulation is regulated. Thyroliberin increases the blood corticotropin content, which causes an elevation of the arterial blood pressure and cerebrovascular tension. On the contrary, in the CSF the corticotropin level decreases after thyroliberin administration. The data obtained show that there is no correlation between the content of beta-endorphine and corticotropin in blood and CSF under the action of thyroliberin.
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PMID:[Brain blood supply and beta-endorphin and corticotropin content on exposure to thyroliberin]. 298 50

We measured CSF and plasma contents of beta-endorphin (beta-EP), beta-lipotropin (beta-LPH), and ACTH in 24 patients with Parkinson's disease; 14 had not been treated. CSF beta-EP concentrations in untreated patients were lower than in 15 controls (p less than 0.005), but values did not differ significantly in treated and untreated patients. In untreated and treated patients, ACTH and beta-LPH CSF, and beta-EP, beta-LPH, and ACTH plasma concentrations were in the same range as controls. The Parkinson's disease-related decrease of CSF beta-EP levels further supports the concept that there is a generalized brain disorder in Parkinson's disease affecting more than dopaminergic neurons in the substantia nigra.
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PMID:beta-Endorphin cerebrospinal fluid decrease in untreated parkinsonian patients. 299 18

The most examined tumor markers in lung cancer patients are CEA, hormonal peptides, and some neurogenic enzymes in small cell carcinoma. Calcitonin, ACTH, ADH, CEA, neurophysin, oxytocin, beta-endorphin, neuron-specific enolase, and CK BB are elevated in serum specimens in 25-75% of cases of small cell carcinoma. The level of these markers is related to the stage of the disease in groups of patients; elevated pretreatment levels decrease with tumor regression. Marker levels are not valid in defining the tumor load and the presence of disease in the individual patient. It has not yet been documented that the markers can be used for clinical decisions on antineoplastic therapy. A recent development is the finding that measurement of CSF and plasma concentrations of ADH, calcitonin, CK BB, bombesin, and neuron-specific enolase may contribute in the diagnosis of CNS metastases including meningeal carcinomatosis.
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PMID:Tumor markers in patients with lung cancer. 300 40

Plasma and CSF beta-endorphin (beta-EP), beta-lipotropin (beta-LPH) and ACTH levels were studied in a group of 25 patients who underwent reversible ischaemic attacks or completed strokes. CSF beta-EP and beta-LPH in ischaemic patients were higher than those of the control population, independently of both clinical reversibility of the cerebral damage, and the time lapse sampling and the acute event. The presence of a CT demonstrable lesion was related to the highest CSF beta-EP levels. These data confirm an involvement of central opioid substances in the phenomena related to brain ischaemia. ACTH levels in the CSF did not differ from the controls; this finding further supports the concept of an independent central secretion of the different pro-opiomelanocortin-related peptides. The peripheral plasma concentrations of beta-EP, beta-LPH and ACTH, were, in contrast, within the normal range, confirming that CSF and plasma contents of pro-opiomelanocortin-related peptides are differently controlled and originate from different sources.
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PMID:CSF and plasma levels of pro-opiomelanocortin-related peptides in reversible ischaemic attacks and strokes. 300 73

Molecular forms of immunoreactive adrenocorticotropin (ACTH), beta-lipotropin (beta-LPH) (beta-endorphin (beta-END), human NH-2-terminal (hNT) of pro-opiomelanocortin (POMC), and gamma-3-melanotropin (gamma-3-MSCH) were studied in plasma, CSF and urine of a patient with Nelson's syndrome by molecular sieving and concanavalin A (Con A)-sepharose chromatography. In the culture tumor medium of the tumor cells, and in the plasma and CSF, these compounds were found mainly in forms corresponding in molecular weight to the authentic peptides, with the exception of gamma-3-MSH. Stimulation of the pituitary tumor by synthetic ovine corticotropin-releasing factor (CRF 1-41) caused a 171-468% increase in vivo (60 min) and 453-953% increase in vitro (3h incubation) in the levels of POMC derived peptides; it increased the relative amount of beta-END in vivo, and that of beta-LPH in vitro. Molecular sieving chromatography of urine samples revealed that beta-LPH and hNT are extensively degraded by the kidney. By contrast, ACTH showed no significant renal degradation before the removal of the pituitary adenoma. However, following pituitary surgery, only smaller fragments of immunoreactive (IR) ACTH were detected in the urine. These results suggest no major abnormal metabolic pathway for POMC in Nelson's syndrome, although the proportions of various peptides derived from the precursor could be different in vivo from those after in vitro incubation under basal conditions and during CRF stimulation. The results also indicate differences in the renal handling of ACTH in POMC hypersecretory states.
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PMID:Characterization of peptides derived from pro-opiomelanocortin in the biological fluids of a patient with Nelson's syndrome. 300 68

We examined corticotropin-releasing hormone-like immunoreactivity (CRH-LI) and corticotropin (ACTH) levels in the CSF of 33 patients with presumptive Alzheimer's disease (AD) and 13 healthy, age-matched controls. The mean CRH-LI and ACTH levels of the AD patients were significantly less than controls. Despite these reductions, none of the patients had evidence of pituitary-adrenal dysfunction. A disorder of extrahypothalamic CRH may be involved in the pathophysiology of AD.
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PMID:Cerebrospinal fluid concentrations of corticotropin-releasing hormone (CRH) and corticotropin (ACTH) are reduced in patients with Alzheimer's disease. 302 28

We measured CSF levels of the opioid peptides beta-endorphin and beta-lipotropin in patients with Alzheimer's disease, multi-infarct dementia and controls. In both dementia groups, the mean concentration of beta-endorphin was significantly lower than in controls. The mean beta-lipotropin levels did not differ significantly in the two groups. The low CSF beta-endorphin level may relate generally to dementia.
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PMID:CSF beta-endorphin and beta-lipotropin in Alzheimer's disease and multi-infarct dementia. 315 72


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