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)

Previous studies have provided evidence of an increased sensitivity to pain, a decreased hypothalamic opioid tone, and decreased cerebrospinal fluid (CSF) beta-endorphin (beta-EP) concentration in patients with primary chronic headache. We applied separate specific radioimmunoassays for beta-EP in CSF and plasma on samples from age-matched controls and a group of 50 patients with chronic tension-type headache (CTH) fulfilling the diagnostic criteria set by the International Headache Society. Median CSF beta-EP concentrations (95% confidence limits) were 12.8 pmol/l (11.0-14.5) in CTH patients and 11.9 pmol/l (10.9-14.2) in the control group, which is not significantly different (P = 0.28). Plasma beta-EP concentrations did not differ either, being 3.1 pmol/l (2.4-3.7) and 3.3 pmol/l (1.8-4.0) in the patients with CTH and in controls, respectively (P = 0.88). Plasma and CSF beta-EP concentrations did not correlate. Reversed-phase high performance liquid chromatography (HPLC) of CSF pools from the headache patients and controls revealed similar profiles of beta-EP-immunoreactivity both when C-terminally and N-terminally directed antisera were used, suggesting a normal post-translational processing of the pro-opiomelanocortin gene in patients with CTH. beta-EP is not involved in the pathogenesis of CTH, or such a role is not reflected in CSF or plasma concentrations of the neuropeptide.
Pain 1992 Nov
PMID:Plasma and cerebrospinal fluid beta-endorphin in chronic tension-type headache. 148 13

Pentobarbital anesthesia causes about a 10-fold increase in the antinociceptive potency of beta-endorphin microinjected into the periaqueductal gray (PAG) region of the rat brain. The antinociceptive response to PAG morphine was markedly attenuated during anesthesia, but returned as the rats regained consciousness. As they recovered from anesthesia, muscular rigidity and body stiffness (catalepsy) also occurred in the pentobarbital treated animals receiving morphine. These results are consistent with the activation of separate and distinct descending pain inhibitory neuronal systems by these two opioid agonists, and the differential modulation of the systems by pentobarbital. They also suggest that the mechanism underlying muscular responses to morphine is sensitive to pentobarbital, and is not shared by beta-endorphin.
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PMID:Antinociception from the administration of beta-endorphin into the periaqueductal gray of rat is enhanced while that of morphine is inhibited by barbiturate anesthesia. 149 80

The effect of LPSw, a lipopolysaccharide from a water extract of wheat flour, on pain response was investigated using an acetic acid-induced writhing test in mice. LPSw inhibited writhing dose-dependently in the range of 10 ng-10 micrograms/mouse i.v. This effect reached its maximum 1.5-3 h after the LPSw inoculation and was detectable even after 8 h. The analgesic effect of LPSw was inhibited by i.v. injection of naloxone and also beta-endorphin was detected in serum and brain tissue following injection of LPSw. Preliminary clinical trials were done in which LPSw was administered percutaneously to relieve the pain of patients with herpes. The results showed that pain was relieved by this application. LPSw may be the best analgesic drug so far known, since it induces the endogenous mediator of analgesia, beta-endorphin.
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PMID:Homeostasis as regulated by activated macrophage. IV. Analgesic effect of LPSw, a lipopolysaccharide of wheat flour. 152 27

Exercise-induced increases in the peripheral beta-endorphin concentration are mainly associated both with changes in pain perception and mood state and are possibly of importance in substrate metabolism. A more precise understanding of opioid function during exercise can be achieved by investigating the changes in beta-endorphin concentrations dependent upon intensity and duration of physical exercise and in comparison to other stress hormones. Published studies reveal that incremental graded and short term anaerobic exercise lead to an increase in beta-endorphin levels, the extent correlating with the lactate concentration. During incremental graded exercise beta-endorphin levels increase when the anaerobic threshold has been exceeded or at the point of an overproportionate increase in lactate. In endurance exercise performed at a steady-state between lactate production and elimination, blood beta-endorphin levels do not increase until exercise duration exceeds approximately 1 hour, with the increase being exponential thereafter. beta-Endorphin and ACTH are secreted simultaneously during exercise, followed by a delayed release of cortisol. It is not yet clear whether a relationship exists between the catecholamines and beta-endorphin. These results support a possible role of beta-endorphin in changes of mood state and pain perception during endurance sports. In predominantly anaerobic exercise the behaviour of beta-endorphin depends on the degree of metabolic demand, suggesting an influence of endogenous opioids on anaerobic capacity or acidosis tolerance. Further investigations are necessary to determine the role of beta-endorphin in exercise-mediated physiological and psychological events.
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PMID:Changes in beta-endorphin levels in response to aerobic and anaerobic exercise. 155 53

Seventy-five consecutive patients undergoing laparoscopy for chronic pelvic pain and/or infertility were studied to test whether beta-endorphin concentrations in peripheral mononuclear cells differed according to the presence or absence of endometriosis. Endometriosis was diagnosed in 45 subjects (minimal in 24, mild in 11, moderate in four, and severe in six). Twenty-eight women (62%) with endometriosis and ten (33%) without the disease reported moderate or severe pelvic pain. beta-Endorphin levels were lower in the endometriosis group than in the controls (16.6 +/- 11.2 versus 21.9 +/- 10.5 pg/10(6) cells; P less than .01). This decrease was attributable to reduced beta-endorphin concentrations in the endometriosis patients with moderate or severe pain compared with symptomatic controls (15.5 +/- 10.0 versus 26.3 +/- 7.0 pg/10(6) cells; P less than .01). A significant difference was also found in relation to the cycle phase: The opioid concentration was reduced in the luteal phase in the endometriosis group compared with controls (14.4 +/- 8.4 versus 23.8 +/- 7.5 pg/10(6) cells; P less than .01), but no differences were demonstrated in the follicular and periovulatory phases. beta-Endorphin is capable of modulating the immune response and can be considered as a classical cytokine. Low beta-endorphin production during the luteal phase may have implications in the development and/or maintenance of endometriosis.
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PMID:Mononuclear cell beta-endorphin concentration in women with and without endometriosis. 156 59

A series of studies with humans as well as experiments carried out on animals could show that physical exercise leads to temporary hypoalgesia. Reduced sensitivity to pain is not only demonstrable after long-distance exercise (such as marathon run) but also after intensive physical exercise on a laboratory ergometer. Pain threshold elevation is most pronounced during maximal exertion, but hypoalgesia remains present also after exercise is stopped demonstrating that a systemic analgetic effect is induced by the exercise process. Pre-exercise pain threshold level is returned to approximately 60 minutes after the exercise. The cause of the exercise-induced hypoalgesia is probably an activation of central pain inhibitory mechanisms by the "stimulus" of physical exercise (stimulation- or stress-induced analgesia). Central pain inhibitory systems are thereby triggered by the stimulation of afferent nerve endings (group III and IV) in the skeletal muscle. The same trigger mechanism also plays a role as a release stimulus for hormones such for beta-endorphin which is increased under physical exercise. Plasma-beta-endorphin is probably not directly involved in the exercise-induced hypoalgesia but is rather a "marker" for the activating of central analgesia mechanisms. Stress-induced hypoalgesia plays also a role in the coronary heart disease. The activation of endogenous analgetic mechanisms leads to a part of the myocardial ischaemia provoked by exercise being silent under exercise. Completely asymptomatic myocardial ischaemia patients display a generalized hypoalgesia which is demonstrable independent of an exertion stimulus and which indicates a central set-point change in the antinociceptive system.
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PMID:Transient hypoalgesia under physical exercise--relation to silent ischaemia and implications for cardiac rehabilitation. 159 Jun 52

Several studies have described changes in beta-endorphin-like immunoreactivity (beta-ELI) in the rat brain in response to pain and stress stimuli. In order to ascertain the components of beta-ELI, brain samples of rats experiencing acute prolonged (tonic) pain were evaluated for their beta-ELI and later submitted to a chromatographic purification allowing the measurement of beta-endorphin (beta-EP) and acetyl beta-EP. The chromatographic analysis of both ventromedial hypothalamus (VMH) and periaqueductal grey (PAG) homogenates indicates that beta-ELI is distributed in several fractions including shortened forms of beta-EP and their respective acetylated compounds. Quantitatively, while beta-ELI in formalin-injected animals was increased by 48% in VMH and 45% in PAG in respect to controls, the net increase of purified beta-EP was 1100% and 470%, respectively, for VMH and PAG. Moreover, the maximal increase of beta-ELI was evident at 120 min, in both tissues. In contrast, the beta-EP peak was reached at 30 min in VMH and at 60 min in PAG. Acetyl beta-EP was unchanged by treatment in both central areas. No correlation of beta-ELI and beta-EP was found in VMH. These data demonstrate that the evaluation of beta-ELI gives a poor estimate of beta-EP changes, due to several components of the endorphin family.
Pain 1992 Apr
PMID:Central changes of beta-endorphin-like immunoreactivity during rat tonic pain differ from those of purified beta-endorphin. 159 71

In several diseases chronic pain is associated with long-lasting pathophysiological responses which differ strongly from those observed in acute situations. When persisting, acute pain often results in physical and psychological stress which may in turn aggravate the initial pathological state. In the present work we examined the secretory patterns of pituitary hormones related to acute stress (growth hormone (GH), prolactin (PRL) and beta-endorphin (beta-END)) in rats during the phase of Freund adjuvant-induced arthritis (AIA, a model used for chronic pain studies) when chronic pain is maximum (14 and 21 days, postinoculation (PI)). Using radio-immunoassay hormones were measured in plasma samples taken every 30 min for 7 h in free-moving rats 14 and 21 days after Freund adjuvant or vehicle injection and in control animals. The total amount of GH secretion was higher at 14 and 21 days PI in AIA rats as compared to vehicle-treated and control animals, and the pulsatility of GH secretory pattern was not modified by AIA. PRL and beta-END secretion were not significantly different in arthritic rats as compared to controls. These results show that GH, PRL and beta-END responses induced by acute stress are not observed during the AIA phase when chronic pain is maximum. Thus, in our experimental conditions, beta-END and PRL do not seem to be good plasma markers of chronic pain.(ABSTRACT TRUNCATED AT 250 WORDS)
Pain 1992 Apr
PMID:Chronic pain induces a paradoxical increase in growth hormone secretion without affecting other hormones related to acute stress in the rat. 159 79

Previous research has suggested that a short-term (6 week) high-intensity and a subsequent long-term (1 year) low-intensity dynamic training programme in 8 patients with rheumatoid arthritis (RA) increased circulating levels of beta-endorphin (beta-EP) during the high-intensity training and of corticotropin-releasing factor (CRF) and beta-lipotropin (beta-LPH) levels during the low-intensity training, without an increase of pain experience. The present follow-up study of the patients, using the data obtained after an additional 1-year period of no standardized training as reference values, indicated that CRF levels decreased significantly (P less than 0.01) in relation to those obtained 1 year earlier. For beta-LPH and beta-EP, no corresponding decreases were noted. No significant difference concerning experience of pain over time was found. High-performance liquid chromatography demonstrated a complex elution pattern with low basal concentration of beta-LPH, which increased after 60 min of training.
Pain 1992 Apr
PMID:Dynamic training and circulating neuropeptides in rheumatoid arthritis: a two-year follow-up study. 159 83

Administration of monosodium glutamate (MSG) in the neonatal period renders the rat to be alpha-MSH deficient later in life. In this study rats received MSG in their neonatal period and were examined at the age of 60 days. alpha-MSH caused hypothermia, potentiated induced hypothermia, blocked paradoxical behavioral thermoregulation, improved performance in the Morris water tank, but had no effect on pain threshold. Melanin only caused an increase in pain threshold. It is suggested that the differential effect of alpha-MSH and melanin is governed by the dopaminergic system.
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PMID:The facilitative effects of alpha-MSH and melanin on learning, thermoregulation, and pain in neonatal MSG-treated rats. 168 21


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