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)

Levels of beta-endorphin in peripheral blood mononuclear cells have been studied as a new approach to investigating opioid tone in migraine and tension-type headache. Sixty-one patients with migraine without aura, 39 with migraine with aura and 23 with episodic tension-type headache were compared with 37 healthy controls. Peripheral blood samples were taken from patients not enduring headache attacks and not undergoing prophylactic treatment. A significant reduction in peripheral blood mononuclear cell beta-endorphin concentrations was observed in migraine patients with and without aura, but not in tension-type headache patients. Altered transmitter modulation to peripheral blood mononuclear cells may be the cause of this alteration, which could be part of a more diffuse opioid system derangement in migraine subjects.
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PMID:Beta-endorphin concentrations in the peripheral blood mononuclear cells of migraine and tension-type headache patients. 147 44

The somatostatin-like (SLI), the neuropeptide Y-like (NPY-LI), and the beta-endorphin-like (BE-LI) immunoreactivities of cerebrospinal fluid (CSF) obtained by suboccipital puncture, or plasma from patients suffering from common migraine or other neuropsychiatric disorders were analysed. The SLI concentration was tendentiously decreased in the migraine patients during the attack-free period compared to that of a 'mixed neuropsychiatric group'. During the migraine attack the level of SLI was further decreased. Similar alteration was found in the CSF BE-LI, while the BE-LI in the plasma showed only a tendentious decrease in common migraine patients. The NPY-LI did not change during the attack period in the CSF or plasma. These findings may indicate the possible role of somatostatin in the pathogenesis of common migraine, and support earlier observations that beta-endorphin is involved in the development in this disorder.
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PMID:Suboccipital cerebrospinal fluid and plasma concentrations of somatostatin, neuropeptide Y and beta-endorphin in patients with common migraine. 135 79

Beta-endorphin is a peptide with morphine-like effects produced primarily in the anterior lobe of the pituitary gland. After its cleavage from the parent molecule, proopiomelanocortin, beta-endorphin is circulated via the blood stream to interact with specific opioid receptors located throughout the body. The peptide produces analgesia by inhibiting the firing of peripheral somatosensory fibers. It also affects other senses, such as vision, hearing, and smell. Whereas the ability to increase beta-endorphin secretion during times of surgical stress is positively correlated with amelioration of pain, the administration of exogenous opioids, such as fentanyl, reduces plasma beta-endorphin. Decreased beta-endorphin concentrations may play a role in trigeminal neuralgia, migraine headache, and rheumatoid arthritis.
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PMID:Peripheral beta-endorphin and pain modulation. 181 47

In this study we measured concentrations of beta-endorphin, ACTH, prolactin and cortisol in plasma of migraine patients (ages 10-19) and age-matched controls, and the effects of behaviour therapy on both migraine and the endocrine parameters. Two groups of migraine patients (M) and controls (C) were recruited: group I (MI, n = 11; CI, n = 13) in winter and group II (MII, n = 9; CII, n = 7) in summer. Both M groups received behaviour therapy: group MI immediately and group MII after a waiting period of 3.5 months. Hormone determinations were made before and after the behaviour therapy of group MI and before and after the waiting period of group MII. At the first measurement (before therapy and waiting period), migraine subjects had lower concentrations of beta-endorphin than controls. After behaviour therapy, both groups showed a significant decline in migraine, which was retained at follow-up 9-12 months after completion of the therapy. Improvement of migraine after behaviour therapy was accompanied by a rise in the level of beta-endorphin in group MI. In contrast, the patients of the waiting period (group MII) showed improvement in migraine after the waiting period but no changes in beta-endorphin. Seasonal differences were observed for beta-endorphin, prolactin and cortisol, winter values being lower than summer values.
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PMID:Effects of behaviour therapy on migraine and plasma beta-endorphin in young migraine patients. 216 31

Thanks to recent biochemical and neuroendocrine findings, migraine belonging to the group of primary headaches appears as a pathology of the antinociceptive system with evolutive character. It has been demonstrated, in fact, that right at the early stage of migraine, there is a significant reduction in liquoral concentrations of beta-endorphin (beta-E), endogenous opioid peptide followed by a similar change in the plasma opioid system. The opioid system deficiency is even more evident after stimulation tests that point to reduced reactivity of the hypothalamo-hypophyseal system with respect to stimuli that in normal subjects trigger hypophyseal beta-E incretion. Caffeine, a member of the methyl-xanthine group, is an interesting molecule in the study of migraine patients because the chronic intake of this substance, contained in numerous analgesics, has been related to the chronic nature of the pain. The purpose of the present study is to assess the relationship between caffeine consumption and plasma opioid system. With the administration of a single oral dose of caffeine, normal subjects present an increase in plasma concentrations of beta-E, while in patients with chronic migraine, the response is significantly lower. These data confirm the poor reactivity of the plasma opioid system to pharmacological stimuli in migraine. Average daily consumption of caffeine has also been determined. It was not possible to establish a correlation between consumption of caffeine and plasma concentrations of beta-E whether basal or after stimulus with caffeine.
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PMID:[Plasma beta-endorphin and caffeine consumption in chronic hemicrania]. 223 63

The effects of naloxone and a met-enkephalin analogue on head pain, vascular responses, and autonomic-associated symptoms were studied in 24 migraine patients, 12 patients suffering from tension-type headache, and 24 normal subjects in whom headache was induced by intravenous injections of increasing doses of histamine (histamine test). A hypersensitivity to histamine was found in migraine patients. Naloxone slightly increased the intensity of pain in migraine and tension-type headache sufferers. The met-enkephalin analogue did not affect the intensity of pain in migraine patients, tension-type headache patients, and normal subjects, but it reduced the intensity and duration of facial flushing (p less than 0.001) and the autonomic symptoms (p less than 0.001) in migraine patients when the pretreatment was not given shortly before histamine. In migraine patients, there seems to be an increased reactivity (receptor supersensitivity?) to the met-enkephalin analogue at the level of systems that inhibit facial vasodilatation and autonomic symptoms.
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PMID:Increased reactivity to a met-enkephalin analogue in the control of autonomic responses in migraine patients. 227 18

To assess the biological correlates of the precipitation of migraine attacks in the perimenstrual period, plasma beta-endorphin (beta-EP) and cortisol responses to naloxone (8 mg iv) and corticotropin releasing hormone (100 micrograms iv) were evaluated in both the follicular phase and the premenstrual period in 7 patients suffering from menstrual migraine and in 7 healthy, asymptomatic control volunteers. In the controls, naloxone evoked a significant release of both beta-EP (F = 5.86, p less than 0.002) and cortisol (F = 4.43, p less than 0.008), independently of the menstrual cycle phase (F = 0.31 and 1.04, for beta-EP and cortisol, respectively). Menstrual migraine patients, on the other hand, showed a significant hormone response only in the follicular phase, not in the premenstrual period. Corticotropin releasing hormone significantly increased beta-EP and cortisol in both the controls and the menstrual migraine patients, independently of the menstrual cycle phase. In both the naloxone and corticotropin releasing hormone testings, the basal beta-EP levels measured in the premenstrual period were lower than those observed in the follicular phase (p less than 0.02). These data demonstrate a cyclical, premenstrual dysfunction of the hypothalamic control exerted by opioids on the hypothalamus-pituitary-adrenal axis. Impairment of this fundamental adaptive mechanism (involved in stress responses and in pain control) could establish a causal relationship between menstrual-related migraine attacks and premenstrual opioid hyposensitivity.
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PMID:Opioid control of the hypothalamus-pituitary-adrenal axis cyclically fails in menstrual migraine. 231 51

To evaluate the change of the neurotransmitter function in migraine, a neuroendocrinological study was performed in eleven female migraineurs and nine female controls. Thyrotropin releasing hormone, luteinizing hormone releasing hormone, and insulin were simultaneously loaded (the Triple test). Before and after loading, serum glucose, prolactin (PRL), thyroid stimulating hormone (TSH), luteinizing hormone, follicle stimulating hormone, adrenocorticotropic hormone, cortisol, human growth hormone and beta-endorphin were measured. The Triple test produced an increase of PRL in both migraine and control groups, but in migraineurs the increase was significantly larger than in controls. TSH also increased in response to the test, but the TSH response in patients was less than in controls, although not significantly so. The responses of other substances showed no significant differences between the two groups. Although dopaminergic hypofunction in migraine has been proposed by some authors, the present findings rather suggest a serotonergic hyperfunction.
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PMID:A neuroendocrinological study in female migraineurs: prolactin and thyroid stimulating hormone responses. 250 60

Blood plasma beta-endorphin concentrations were measured in 87 patients with various facial and head pain syndromes: trigeminal neuralgia or neuropathy Horner syndrome and migraine, facial autonomic pains. beta-endorphin concentrations were measured before and after treatment. In the groups under investigation, the neuropeptide showed opposite changes in plasma levels after the therapy depending on the type of the syndrome.
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PMID:[Beta-endorphin levels in patients with pain syndromes in the areas of the face and head]. 253 37

In nine women suffering from menstrual migraine (MM), and in six healthy asymptomatic volunteers, plasma beta-endorphin (beta-EP), growth hormone (GH), norepinephrine (NE), and 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) concentrations were measured in response to clonidine (0.075 mg, i.v.) stimulation. In MM patients clonidine testing was performed in both the early and the late luteal phases of the menstrual cycle. Premenstrual symptoms were prospectively evaluated in the actual cycle using the Moos Menstrual Distress Questionnaire. beta-EP (after gel chromatography) and GH were measured using radioimmunoassay. NE and MHPG were evaluated by HPLC using electrochemical detection. In both phases of the menstrual cycle clonidine significantly reduced NE and MHPG levels in MM patients and controls in a similar way. In MM patients beta-EP and GH plasma levels were stimulated by clonidine only in the early luteal phase, whereas they remained unchanged when they were stimulated in the premenstrual period. In controls the response of both hormones was not affected by the menstrual cycle. The lack of hormonal response to clonidine in MM may suggest a postsynaptic alpha 2-adrenoreceptor hyposensitivity during the premenstrual period. This demonstrates a transient vulnerability of the neuroendocrine/neurovegetative systems, and could thus be a factor facilitating the precipitation of both behavioral changes and migraine attacks.
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PMID:Premenstrual failure of alpha-adrenergic stimulation on hypothalamus-pituitary responses in menstrual migraine. 255 88


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