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 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

The present study was designed to determine the effects of partial cholinergic denervation on parietal cortical corticotropin-releasing hormone-like immunoreactivity (CRH-LI) in the rat at different ages. Young adult rats received either unilateral or bilateral ibotenic acid infusions into their nucleus basalis, destroying most of the acetylcholinesterase-positive neurons in that region. Parietal cortical levels of CRH-LI were assayed 2.5, 10, 14 and 19 months after placement of nucleus basalis lesions. Parietal CRH-LI was elevated at 10, 14 and 19 months in bilaterally lesioned animals, while unilateral lesions had no effect on CRH-LI.
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PMID:Effects of nucleus basalis lesions on cerebral cortical concentrations of corticotropin-releasing hormone (CRH)-like immunoreactivity in the rat. 237 21

Immunoreactive corticotropin-releasing hormone (IR-CRH) in maternal plasma increases progressively during pregnancy and decreases rapidly after delivery, suggesting that IR-CRH is produced in the placenta. We studied the expression of the CRH gene in developing human chorionic tissue, the amniotic membrane, the uterine myometrium and a fresh surgical specimen of hydatidiform mole by Northern blot analysis. Our results were as follows: (1) CRH mRNA was demonstrated in the placenta in the third trimester and at term, but under detectable level in the first and second trimesters. (2) CRH mRNA expression was observed in the amniotic membrane, but its expression in the myometrium in normal pregnancy was under detectable level at term. (3) CRH mRNA was also under detectable level in trophoblasts of a hydatidiform mole. These results suggest that the sources of the increased level of IR-CRH in human plasma and amniotic fluid during pregnancy are the placenta and amniotic membrane, and that gene expression of placental CRH increases during pregnancy.
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PMID:Expression of the corticotropin-releasing hormone (CRH) gene in human placenta and amniotic membrane. 240 49

Corticotropin-releasing hormone, a 41-amino-acid peptide, is an important hypothalamic factor regulating the pituitary secretion of adrenocorticotropic hormone (ACTH). This hormone, while rarely involved in the etiology of Cushing's syndrome, seems to play a major role in the pathogenesis of non-Cushing hypercortisolemic states. The administration of synthetic human and ovine CRH has been found useful in the differential diagnosis of Cushing's syndrome and in the preoperative localization of intrasellar ACTH-secreting tumors.
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PMID:Corticotropin-releasing hormone: clinical applications. 254 67

Observations of neuropsychiatric changes in patients receiving interleukin-2 (IL-2) led us to examine the effects of IL-2 administration on the stress-related hormones, beta-endorphin, ACTH, cortisol, and CRH. We evaluated 30 cancer patients who received immunotherapy with IL-2 or IL-2 plus lymphokine-activated killer (LAK) cells. Blood samples were taken immediately before and 4 and 8 h after infusion of IL-2 or IL-2 plus LAK cells. IL-2 stimulated increased hormone levels 4 h after infusion compared with those before therapy and with basal levels in normal volunteers at the following magnitudes: beta-endorphin, 10-fold; ACTH, 20-fold; and cortisol, 2-fold. The effect of IL-2 was not altered in patients also receiving LAK cells. An effect of treatment course was noted, with higher stimulated values seen 4 h after IL-2 in the second treatment course compared with those after the first course [change (delta) in beta-endorphin, 101 vs. 11 fmol/mL; delta ACTH, 138 vs. 8 pmol/L; delta cortisol, 414 vs. 218 nmol/L]. We conclude that IL-2 treatment induces the release of neuroendocrine hormones and that a significant increase in hormonal stimulation occurs upon reexposure to IL-2.
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PMID:The neuroendocrine effects of interleukin-2 treatment. 254 65

Since the discovery of CRH in 1981, several investigators have reported abnormalities of the hypothalamic-pituitary-adrenal (HPA) system in response to direct stimulation of the corticotroph cells in patients with psychiatric disorders. To further explore HPA system integrity in major depressive disorders, 13 drug-free patients and normal subjects matched for age, sex, ovarian status, and body weight received 100 micrograms synthetic human CRH as an iv bolus dose. Compared to that in the normal subjects, in the depressed patients a significant attenuation of the net ACTH release after CRH administration (772 +/- 597 vs. 263 +/- 286 pmol/min.L; P less than 0.02) was observed, while beta-endorphin and cortisol responses did not differ significantly between the groups. The magnitudes of ACTH and cortisol release were negatively correlated in the patient group only (r = -0.67; P less than 0.01). Thus, the blunted ACTH response to CRH in depression might be related to hypercortisolemia, while the implications of the apparent dissociation of ACTH and beta-endorphin after CRH administration still remain unclear. Our data support the hypothesis that the hyperactivity of the HPA system in depression most likely is a consequence of CRH hypersecretion, the origin of which may be explained by abnormal central glucocorticoid receptor or neurotransmitter regulation.
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PMID:Blunted adrenocorticotropin but normal beta-endorphin release after human corticotropin-releasing hormone administration in depression. 254 28

Ether and restraint stress-induced peripheral plasma corticotropin releasing hormone (CRH), arginine vasopressin (AVP), oxytocin (OXY) and adrenocorticotropin (ACTH) levels were measured by radioimmunoassays. Plasma CRH, AVP, OXY and ACTH rose to approximately twice the level of control rats 2 min after the onset of a 1-min exposure to ether. Plasma CRH rose further 5 min after the onset of ether stress, while plasma AVP and OXY returned to the baseline levels at 5 min. Plasma CRH, OXY and ACTH showed significant elevation 2 min after the onset of restraint stress, while plasma AVP did not show a significant change. Plasma OXY and ACTH rose further 5 min after the onset of restraint stress, whereas plasma CRH returned to baseline levels. CRH and OXY concentrations in the hypothalamic median eminence decreased 5 min after the onset of ether exposure and restraint, while the AVP concentration did not differ from control levels. The results, including the discrepancy between plasma CRH and ACTH 5 min after stress, suggest that CRH in the peripheral plasma is derived from both hypothalamic and extrahypothalamic tissues. The levels of stress-induced CRH in the peripheral plasma were sufficient to stimulate ACTH release. These results suggest that ether and restraint stress elevate plasma CRH shortly after the onset of the stress, and that this elevation in the plasma CRH level is at least partly responsible for stress-induced ACTH secretion.
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PMID:Effect of acute ether or restraint stress on plasma corticotropin-releasing hormone, vasopressin and oxytocin levels in the rat. 254 72

To determine whether CRH affects adrenal androgen, beta-endorphin (B-E), and ACTH secretion in normal children during sexual maturation, 17-hydroxyprogesterone (17-OHP), androstenedione (D4-A), dehydroepiandrosterone (DHEA), DHEA sulfate (DS), cortisol, B-E, and ACTH were measured after an iv injection of 1 microgram/kg human CRH. Children with premature pubarche were similarly analyzed to establish whether this condition is accompanied by altered hormonal responses to CRH. CRH produced consistent increases in ACTH, B-EP, and cortisol blood levels, which were comparable at all age intervals in all groups. 17-OHP increased after CRH injection, but its response linearly with age. D4-A levels were not influenced, while DHEA and DS levels were only partially influenced by CRH. The stimulated D4-A to 17-OHP ratio increased with sexual maturation, whereas ratios of cortisol to 17-OHP and D4-A to DHEA remained constant. Children with premature pubarche had hormonal responses similar in magnitude to those of prepubertal children of comparable age. In conclusion, an increase in 17,20-desmolase efficiency occurs with postnatal maturation after CRH challenge. Moreover, CRH does not appear to play an important role in premature pubarche.
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PMID:Adrenal steroid, cortisol, adrenocorticotropin, and beta-endorphin responses to human corticotropin-releasing hormone stimulation test in normal children and children with premature pubarche. 255 May 9

Seven cases with uremia (6 men, 1 woman, mean age = 55.6 +/- 2.2 years) were studied with four combined hypothalamic releasing hormones (corticotropin-releasing hormone, CRH; luteinizing hormone-releasing hormone, LHRH; thyrotropin-releasing hormone, TRH; and growth hormone-releasing hormone, GHRH) for assessment of anterior pituitary functions. The mean basal levels of corticotropin (ACTH, 22.4 +/- 5.2 pg/ml), thyrotropin (TSH, 2.4 +/- 0.6 microU/ml), and follicle stimulating hormone (FSH, 26.0 +/- 3.4 mIU/ml) in uremic patients were not significantly different from those (34.0 +/- 3.5 pg/ml, 2.0 +/- 0.4 microU/ml, and 23.2 +/- 6.4 mIU/ml) of controls (5 men, 1 woman, mean age = 54 +/- 2.5 years), but the ACTH and TSH responses to the releasing hormones were significantly lower than those of the controls. The mean basal levels of luteinizing hormone (LH, 70.7 +/- 16.3 mIU/ml), cortisol (9.8 +/- 1.2 micrograms/dl) and prolactin (109.3 +/- 23.2 ng/ml) in uremic patients were significantly higher than those of normals (27.3 +/- 6.6 mIU/ml, 6.5 +/- 0.7 micrograms/dl and 15.7 +/- 3.4 ng/ml), while suppressed LH, cortisol and prolactin responses to the releasing hormones were observed in the uremic group. The mean basal growth hormone (GH) level in uremic patients (3.1 +/- 0.4 ng/ml) was not significantly different from that (2.8 +/- 0.7 ng/ml) of normals, but the GH response to the releasing hormones was significantly higher than that of controls. These results show pituitary dysfunction, such as blunted ACTH, TSH, LH and prolactin response, exists in uremic patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Anterior pituitary functions in patients with uremia tested by stimulation with four combined hypothalamic releasing hormones. 256 85

Twenty subjects (10 patients with a major depressive episode and 10 individually matched healthy controls) received 100 micrograms synthetic human corticotropin-releasing hormone (hCRH) as an i.v. bolus dose. Healthy subjects and depressed patients exhibited a significant increase of plasma somatostatin (SRIH) concentrations with no difference between both comparison groups. Compared to controls, depressed patients showed a significant attenuation of corticotropin (ACTH) responses, while cortisol secretion in response to hCRH was normal. No correlations were found among basal plasma concentrations of SRIH, ACTH or cortisol and SRIH, ACTH or cortisol responses following hCRH. These findings are compatible with the hypothesis that hypothalamic-pituitary-adrenal (HPA) hyperactivity in the depressive state may primarily be due to central hypersecretion of CRH and support the view of a hCRH-induced SRIH secretion which is not related to HPA dysfunction associated with major depression.
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PMID:The influence of human corticotropin-releasing hormone on somatostatin secretion in depressed patients and controls. 256 52


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