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)

A 28 year-old woman was admitted to Jichi Medical School Hospital because of amenorrhea, cold intolerance, easy fatigability and body weight loss. She was pregnant at the age of 26 years. She delivered a 3230 g healthy girl at full term without any complications. However, she did not have any lactation or recurrence of menstruation after the delivery. Serum cortisol was 0.7 micrograms/dl, and plasma adrenocorticotropic hormone (ACTH) was less than 10 pg/ml. Both hormones failed to increase in response to insulin-induced hypoglycemia or exogenous arginine vasopressin. However, serum cortisol and urinary excretion of 17-hydroxycorticosteroids (17-OHCS) were significantly increased by the repeated administration of ACTH. Serum prolactin was 2.2 ng/ml and the level did not rise after the administration of thyrotropin releasing hormone (TRH). Responses of release of adenohypophysial hormones including gonadotropins, growth hormone and thyroid stimulating hormone (TSH) were normal. Serological studies showed an antibody to the pituitary gland which was demonstrated by an indirect immunofluorescence technique. Plain skull X-ray film and brain computerized tomography revealed an empty sella of the normal size. These results indicate the presence of partial deficiency of ACTH and prolactin, and that autoimmune disorders may be involved in the pathogenesis of her hypopituitarism.
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PMID:A case of partial hypopituitarism with empty sella following normal course of pregnancy and delivery. 301

The plasma concentrations of adrenocorticotropic hormone (ACTH) in rats pretreated with capsaicin as neonates were compared with those of control rats pretreated with the capsaicin vehicle. Capsaicin pretreatment has been shown earlier to abolish the increase in plasma ACTH concentration induced by cold stress while not affecting that induced by restraint stress. In the present experiments rats pretreated with capsaicin showed the same increase in plasma ACTH concentration in response to an i.v. infusion of ovine-corticotropin releasing factor as control rats pretreated with the capsaicin vehicle. Intraperitoneal injection of formalin, surgical stress and intravenous infusion of (-)-isoprenaline increased plasma ACTH concentrations in control rats. In capsaicin pretreated rats the increase in plasma ACTH was significantly attenuated. It is concluded that capsaicin-sensitive sensory neurones mediate the activation of pituitary ACTH secretion in response to somatosensory stimuli. The function of the corticotroph cells of the anterior pituitary is not impaired by capsaicin treatment.
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PMID:Stress induced ACTH release in capsaicin treated rats. 303 68

Multiple pain-inhibitory systems dependent upon both opioid and nonopioid mechanisms of action have been identified, particularly in the rodent. The experimental subject has typically been the young, adult male rat, and generalizations concerning these systems have been made from this subject pool. This review focuses upon the roles of two organismic factors, aging and gender, in the modulation of analgesic processes. Using an array of age cohorts (4, 9, 14, 19, 24 months), these data illustrate that aging produces differential decrements in the analgesic responses following morphine, different parameters of footshock, continuous cold-water swims (CCWS: a nonopioid stressor), intermittent cold-water swims (ICWS: an opioid stressor) and 2-deoxy-D-glucose (a mixed opioid/nonopioid stressor). In contrast, neither beta-endorphin nor food deprivation analgesia is affected by aging. This review identifies that CCWS and ICWS analgesia are sensitive to gender differences, gonadectomy differences and steroid replacement differences such that females display less analgesia than males, gonadectomy reduces both analgesic responses, and that testosterone is most effective in reinstating gonadectomy-induced analgesic deficits. These data are considered in terms of therapeutic implications for the organismic variables under study as well as for the conceptual and methodological modifications that must be made in studying intrinsic pain inhibition.
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PMID:Organismic variables and pain inhibition: roles of gender and aging. 306 44

An association between increased blood pressure levels and hypoalgesia has been reported in the experimental animal and in man. The relation between pain perception and cardiovascular function is however still obscure. In order to gain some insight into this aspect, normotensive subjects with low and high tolerance to pain, as assessed by tooth pulp stimulation, were compared for blood pressure and heart rate during cold pressor test, 24 hr urinary catecholamines, supine and upright PRA and plasma beta-endorphin levels. No significant difference was observed between the two groups for casual blood pressure, heart rate and PRA. Compared to subjects with low tolerance to pain, those with high tolerance to pain were significantly older and had: 1) significantly higher levels of diastolic blood pressure and of beta endorphin levels during cold pressor test; 2) significantly higher beta-endorphin levels after cold pressor test; 3) a significantly higher excretion of noradrenaline (but not of adrenaline and dopamine).
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PMID:Relationship between pain sensitivity, cardiovascular reactivity to cold pressor test and indexes of activity of the adrenergic and opioid system. 307 26

After injection of 5 micrograms into a lateral cerebral ventricle, 6 of 12 peptides induced mean changes of 0.3 degree C or more in rectal temperature of rabbits. When beta-endorphin was studied further with 1.25-5 micrograms in 10, 23 and 30 degrees C environments, it induced dose-related hypothermia in the cold, hyperthermia in the heat and progressively smaller increases in body temperature with increasing doses at 23 degrees C.
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PMID:Altered body temperature of rabbits after central injection of beta-endorphin and other peptides. 315 76

In 8 young and 8 elderly subjects mean values of plasma beta-endorphin were nearly equal under basal conditions. In all subjects the cold pressor test provoked a marked increase of beta-endorphin, which was more evident in young subjects. Mean values of the areas of endorphin modifications were the same in both young and elderly subjects. These results may suggest that after a short-term stimulus, such as the cold pressor test, no marked differences in pituitary secretion between young and elderly subjects may be evidenced.
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PMID:Beta-endorphin and cold pressor test in the aged. 315 75

Endogenous opioid peptides have been implicated in stress-induced analgesia and stress-induced feeding behavior. An earlier study from our laboratory showed that rats subjected to cold swim stress consumed significantly more food compared to controls. The present study describes changes in the levels of various opioid peptides in the central nervous system and periphery due to cold swim stress. Male Sprague-Dawley rats were subjected to cold swim stress (1 degree C for 5 min), then sacrificed by decapitation; brain, pituitary, adrenals and plasma were collected. Tissue extracts were assayed for opioid peptides by RIA. Cold swim stress resulted in analgesia which could be blocked by prior administration of naloxone, as observed by a tail-flick latency test. Cold swim stress caused a 42% decrease in pituitary beta-endorphin, but increased the level of this peptide in the hypothalamus and plasma by 36% and 337%, respectively. Dynorphin level decreased by 62% in the hypothalamus, but was not affected in the pituitary. Levels of Leu-enkephalin and Met-enkephalin decreased in the adrenal gland by 37% and 18%, respectively, but were not significantly affected in the CNS. These results indicate that cold swim stress has a differential effect on the level of CNS and peripheral opioid peptides, and that both central and peripheral opioid peptides may be important in stress-induced analgesia and feeding behavior.
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PMID:Cold swim stress-induced changes in the levels of opioid peptides in the rat CNS and peripheral tissues. 335 22

The gastrointestinal motor function in patients with anorexia nervosa is poorly understood, although it may be relevant to the pathophysiology of the disorder. We have undertaken a multidisciplinary study of 8 patients with anorexia nervosa and 8 age- and sex-matched controls. We have characterized their gastrointestinal and neurohormonal function by measuring (a) gastric electrical activity, (b) antral phasic pressure activity, (c) gastric emptying of solids and liquids, and (d) hormonal and autonomic function. Patients with anorexia nervosa at the time of the initiation of therapy presented with (a) increased episodes of gastric dysrhythmia (mean percentage of dysrhythmic time: 9.75 patients vs. 0.48 controls during fasting, p less than 0.02; 7.21 patients vs. 0.18 controls postcibally, p less than 0.001), (b) impaired antral contractility (mean motility index, 12.8 patients vs. 14.2 controls, p less than 0.002), (c) delayed emptying of solids, (d) decreased postcibal blood levels of norepinephrine and neurotensin (levels of beta-endorphin, insulin, glucagon, gastric inhibitory polypeptide, gastrin, cholecystokinin, and human pancreatic polypeptide were normal), and (e) impaired autonomic function (resting diastolic blood pressure and skin conductance were decreased and the response to the cold pressor test was dampened). Differences between patient and control groups were statistically significant. We conclude that patients with anorexia nervosa present multiple gastrointestinal abnormalities involving control mechanisms as well as target organs.
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PMID:Gastric electromechanical and neurohormonal function in anorexia nervosa. 365 45

Centrally administered neuropeptides were investigated for their effects on the development of gastric lesions in rats. Thyrotropin releasing hormone (TRH), vasoactive intestinal peptide (VIP) and gonadotropin releasing hormone (LHRH) produced gastric lesions acutely, with TRH demonstrating the most pronounced effect in terms of incidence and severity. Ten-fold higher doses of the same peptides administered intravenously produced none or very few gastric lesions. Moreover, pretreatment with atropine partially inhibited their production. Corticotropin releasing factor (CRF) exhibited only mild ulcerogenic effects, and the gastric lesions induced with this peptide developed more slowly than with TRH, VIP and LHRH. Although ulcerogenic in their own right, none of these four neuropeptides significantly potentiated the potent ulcerogenic effects of cold-restraint stress. Since other neuropeptides, including somatostatin, human pancreatic growth hormone releasing factor (hpGRF), substance P, bombesin, and neurotensin, had no demonstrable effects on gastric mucosa, we can conclude that the lesions were not a general effect of intracisternal administration of neuropeptides. The results suggest that within the central nervous system, there are several neuropeptides that play a significant role in the development of gastric lesions via, at least in part, vagal-dependent mechanisms.
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PMID:The effects of centrally administered neuropeptides on the development of gastric lesions in the rat. 392 Apr 62

Our previous findings that the degree of endotoxin-induced hypotension in the dog is inversely related to ambient temperature (19 degrees through 30 degrees C) and that only increased doses of naloxone are effective at 19 degrees C suggested that opioid activity is also influenced by ambient temperature, increasing in the cold and decreasing in the warm. Others have reported increases in plasma beta-endorphin in rats with acute exposure to both 5 degrees and 36 degrees C. In this study we measured changes in pain thresholds after both acute and chronic exposures to lesser alterations in ambient temperature as a potentially more sensitive index of changes in central opioid activity. Compared to 24 degrees C there was a marked increase in pain threshold with acute exposure to 10 degrees C and marked decreases at 30 degrees and 35 degrees C. A slight decrease occurred after 30 minutes but not 60 or 120 minutes at 19 degrees C. All acute changes disappeared three hours after the animals had been returned from the altered ambient temperature to 24 degrees C. No changes were observed after six days chronic exposure to 10 degrees or 30 degrees C. These findings suggest that moderate, acute changes in ambient temperature can produce inversely related, adaptable alterations in central opioid activity.
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PMID:Pain threshold changes induced by acute exposure to altered ambient temperatures. 404 80


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