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)

1. Basal and haemorrhage-stimulated erythropoietin (Epo) and ACTH levels were measured in the chronically cannulated immature ovine foetus (less than 125 days) by radio immunoassay (RIA). 2. Basal erythropoietin levels were found to be higher than those previously reported in the late gestation (greater than 130 days) ovine foetus, but were lower than those observed in the neonatal lamb. 3. In control foetuses (Protocol 1) the small degree of haemorrhage associated with the sampling procedure increased the plasma Epo values from 11.4 +/- 3.0 (n = 5) mU/mL to 23.8 +/- 4.3 mU/mL at 24 h (mean +/- s.e.m.). There was a significant monotonic increase with time (F = 16.4; d.f. 1,19; P = 0.001). An initial haemorrhage of approximately 10% blood volume (Protocol 2) increased plasma Epo values from 7.3 +/- 2.3 to 24.2 +/- 7.1 mU/mL (n = 3). 4. Haemorrhage of 20% fetal blood volume (Protocol 3) produced an increase in plasma Epo from 9.3 +/- 1.7 to 54.7 +/- 15.5 mU/mL at 6 h and to 57.6 +/- 7.3 mU/mL at 24 h (n = 5). By repeated measures ANOVA, the effect of the 20% haemorrhage was significant when compared with the control group (F = 7.32, d.f. 2,16, P = 0.006). There was a significantly greater decrease in haematocrit (F = 6.7, d.f. 2,20, P = 0.004) and haemoglobin (F = 5.0, d.f. 2,20, P = 0.013) in animals of Protocol 3 than in those of Protocol 1. 5. Fetal blood gases and plasma adrenocorticotropic hormone (ACTH) did not alter with haemorrhage, indicating the tolerance of the foetus to this degree of haemorrhage.
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PMID:The effect of graded haemorrhage on erythropoietin production in the immature ovine foetus. 132 38

Hormones of the hypothalamo-pituitary-adrenocortical (HPA-) axis are considered to be of physiological and clinical relevance in regulating spontaneous growth hormone (GH) secretion. To further investigate interdependencies between both systems, we studied the effects of adrenocorticotropin [ACTH(1-24)] and human corticotropin-releasing hormone (h-CRH) upon spontaneous GH secretion in 10 male volunteers. Administration of 1 microgram ACTH (1-24), 10 micrograms h-CRH or saline (control: CTL) every hour from 9.00 to 6.00 p.m. resulted in significant differences of cortisol secretion during the entire observation period (8.00 a.m.-3.00 a.m.) between the three groups (p less than 0.001, Friedman two-way ANOVA). Mean area under the time course curve (AUC) values (+/- SEM) for cortisol expressed as ng x 1,000 x min/ml showed also significant differences between the three treatments from 8.00 a.m. to 3.00 a.m.: CTL 64.0 +/- 6.4, ACTH(1-24) 178.5 +/- 9.4 (p less than 0.01, Wilcoxon test), h-CRH 88.5 +/- 5.6 (p less than 0.01). The main portion of cortisol was released during daytime from 8.00 a.m. to 11.00 p.m., where the most significant differences in the AUC values emerged: CTL 59.6 +/- 5.8, ACTH(1-24) 171.5 +/- 8.8 (p less than 0.01, Wilcoxon test), h-CRH 80.2 +/- 5.1 (p less than 0.01). With regard to GH secretion, significant differences became obvious between the three treatments during daytime from 8.00 a.m. to 11.00 p.m. and the sleep-related period from 11.00 p.m. to 3.00 a.m. (p less than 0.01 and p less than 0.02, Friedman two-way ANOVA).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of human corticotropin-releasing hormone and adrenocorticotropin upon spontaneous growth hormone secretion. 174 61

Experimental pain thresholds (electrical intracutaneous finger and dental pulp stimulation) and plasma hormone levels (beta-endorphin, cortisol, and catecholamines) were measured in ten healthy sportive men before, during, and after progressively more strenuous physical exercise. In a double-blind study conducted on two different days, 20 mg of the opioid-antagonist naloxone or placebo was administered prior to exercise. A significant pain threshold elevation was found during exercise for finger (ANOVA, P less than 0.004) and dental pulp stimulation (P less than 0.01). Pain threshold elevation was most pronounced during maximal exertion, at which time the subjects reported the greatest subjective fatigue. Thresholds remained elevated 10-15 min after the end of exercise, and, 60 min after exercise, thresholds returned to baseline values. The subjective magnitude estimation of suprathreshold stimuli was significantly reduced (P less than 0.0001) 5-10 min after exercise. Plasma beta-endorphin, cortisol, and catecholamines increased significantly (P less than 0.0005, all values) during exercise. Plasma beta-endorphin levels did not correlate significantly with pain thresholds (r = -0.37, NS). Naloxone failed to affect pain thresholds, although beta-endorphin and cortisol increased significantly more (P less than 0.02) during exercise after naloxone. It is concluded that short-term, exhaustive physical exercise can evoke a transient elevation in pain thresholds. This exercise-induced elevation in pain threshold does not, however, appear to be directly related to plasma endorphin levels.
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PMID:Experimental pain thresholds and plasma beta-endorphin levels during exercise. 202 Feb 72

To explore causal links between vital sign responses and immunoreactive beta-endorphin ("i-BE") rises in blood and CSF during ovine endotoxin stress, we analyzed concurrent i-BE levels in these two compartments by a "vector-ARMA" (= autoregressive moving average) method. This technique--widely used for modeling in other applications--has not to our knowledge been employed to study dynamic relationships of neuropeptides. Log-transformed i-BE levels were first "filtered" by repeated observations ANOVA to confirm significance of rises in both compartments. Next, vector-ARMA methodology was applied to derive an optimal causal model of vital sign changes and i-BE entry into plasma vs. CSF pools. The model indicated that reflux of i-BE from blood into CSF contributed to increases in CSF levels of this hormone. This novel application to neuroendocrinology of this approach illustrates its utility in evaluating changes in one or more neuropeptide levels in multiple compartments to indicate potentially causal relationships.
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PMID:Causal links between plasma and CSF endorphin levels in stress: vector-ARMA analysis. 293 75

Immunoreactive plasma beta-endorphin level was assayed in 33 patients with major affective disorder and in 16 psychiatrically normal controls before and after dexamethasone (1 mg) administration at 23.00 h. There were 18 cortisol suppressors and 15 non-suppressors among the patient group. All controls suppressed cortisol. Plasma beta-endorphin before dexamethasone was significantly different between suppressors, non-suppressors and controls (P less than 0.05, ANOVA). Concentrations of beta-endorphin were 4.7 +/- 0.7, 3.1 +/- 0.3 and 2.8 +/- 0.3 pmol/l for non-suppressors, suppressors and controls respectively. Following dexamethasone, beta-endorphin concentrations were again significantly different between groups (P less than 0.005, ANOVA). Concentrations were 4.6 +/- 0.7, 2.3 +/- 0.2 and 1.6 +/- 0.2 pmol/l for non-suppressors, suppressors and controls respectively. The implications of these findings are discussed.
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PMID:Plasma immunoreactive beta-endorphin in dexamethasone suppressors and non-suppressors of cortisol. 303 84

The aim of the present investigation was to compare the changes in plasma estradiol (E2), progesterone (P), luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone (T), androstenedione (delta 4-A), dehydroepiandrosterone sulfate (DHEA-S), adrenocorticotropic hormone (ACTH), and prolactin (PRL) in standardized tests (15-min consecutive work loads of 60%, 70%, 80% VO2 max to exhaustion) in 13 eumenorrheic untrained (UT) and 8 highly trained women (MR). Blood was obtained 15 and 2 min before exercise and at the end of each work load or each 15 min period. The results showed a significant increase (0.05 greater than P less than 0.001, two-way ANOVA) in plasma E2 P, T delta 4-A, PRL, and ACTH both in UT and MR irrespective of the phase of the menstrual cycle. DHEA S levels increased significantly in the MR, but not in the UT, PRL and ACTH increased linearly with exercise in MR and nonlinearly in UT. In the latter group, only the 80% VO2 max work load was able to elicit significant increments in the plasma levels of these hormones. In the MR plasma T and delta 4-A levels increased relatively more pronounced (P less than 0.05) at comparable work loads and exercise times than in the UT. LH levels decreased with exercise both in the UT and MR, whereas FSH levels remained unchanged (MR) or decreased (UT). These findings suggest that during exercise the ovarian hormones are increased by more unspecific mechanisms such as a decreased metabolic clearance rate, whereas in the MR, adrenal secretion of androgens is enhanced.
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PMID:Multiple hormonal responses to physical exercise in eumenorrheic trained and untrained women. 342 89

Abnormalities in corticotropin-releasing hormone (CRH) secretion, noradrenergic neurotransmission, and serotonergic activity in the central nervous system (CNS) have all been hypothesized to exist in alcoholic patients, as have abnormalities in hypothalamic-pituitary adrenal function. To test these hypotheses, we continuously sampled cerebrospinal fluid (CSF) from alcoholic patients after 38-124 days of abstinence and from normal volunteers via a flexible, indwelling lumbar subarachnoid catheter and measured CRH, norepinephrine (NE), 3-methoxy-4-hydroxyphenylglycol (MHPG), tryptophan, and 5-hydroxyindoleacetic acid (5-HIAA) concentrations at 10-min intervals, from 11:00 through 17:00 h. The spinal canal catheter was inserted at approximately 08:00 h. Serial plasma ACTH, cortisol, and NE concentrations were also measured. A mixed liquid meal was consumed at 13:00 h. CSF CRH concentrations were lower in alcoholic patients than in normal volunteers (26 +/- 15 vs. 60 +/- 30 pg/ml, respectively, p < 0.05 by ANOVA), as were CSF NE levels (0.33 +/- 0.09 vs. 1.15 +/- 0.51 pmol/ml, respectively, p < 0.01). Plasma NE and CSF MHPG levels were normal in the alcoholic patients. CSF tryptophan and 5-HIAA and plasma ACTH and cortisol concentrations did not differ between the groups. These studies extend our finding of reduced spinal canal CSF CRH concentrations in depressed patients to abstinent chronic alcoholics.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Concentrations of corticotropin-releasing hormone, norepinephrine, MHPG, 5-hydroxyindoleacetic acid, and tryptophan in the cerebrospinal fluid of alcoholic patients: serial sampling studies. 753 89

We have reported a decrease in the number of arcuate nucleus (ARC)-immunoreactive beta-endorphin neurons in old (24 months) female C57BL/6J mice versus young (5 months) mice. Here, we have tested by immunocytochemistry whether age-related changes in beta-endorphin neuron numbers are selective for beta-endorphin neurons which do or do not contain estrogen receptors (E2R). We also compared beta-endorphin neuron number in mice with short- (S) and long-duration (L) ovariectomy (OVX), since the latter may protect against neuroendocrine aging. Mice were studied at 5 (young), 12 (middle-aged), or 23-24 months (old). When the mean number of neurons per tissue section (15 sections per animal) was examined, there were no significant differences between young and middle-aged S-OVX females for either beta-endorphin, E2R, or beta-endorphin/E2R neuron number. However, there were significant decreases in beta-endorphin-containing neurons in the oldest age group versus young females (young S-OVX: 74.4 +/- 11 (+/- SD) immunopositive neurons per tissue section, n = 10 mice; young L-OVX: 61.6 +/- 6.9, n = 6; old S-OVX: 45.7 +/- 9.9, n = 7; and old L-OVX: 37.5 +/- 7.3, n = 7). There were also decreases in beta-endorphin neurons which contained E2R in the oldest animals (young S-OVX: 16.6 +/- 6.4; young L-OVX: 13.7 +/- 1.3; old S-OVX: 9.2 +/- 1.8; L-OVX: 6.0 +/- 1.5) (p < 0.05 ANOVA). Both age (p < or = 0.001, two-way ANOVA) and ovarian status (p < or = 0.05) independently affected neuron number for both the beta-endorphin and beta-endorphin/E2R populations versus young mice. We tested whether the observed age and/or ovarian-related decreases were proportionally greater in the subpopulation of beta-endorphin neurons which contained E2R compared to the total beta-endorphin neuron population. In the oldest age group, there was no significant difference in the decrease with age in the population of beta-endorphin neurons which contained E2R and the total beta-endorphin population (p = 0.208). When we examined the E2R neuron population as compared to the beta-endorphin neuron populations, age-related decreases in the beta-endorphin neuronal population tended to be greater than the decreases seen in the E2R neuron population (p = 0.054 repeated measures ANOVA). The tyrosine hydroxylase (TH) neuron population was studied to test whether there were changes in another ARC neuron population.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of age and long-term ovariectomy on the estrogen-receptor containing subpopulations of beta-endorphin-immunoreactive neurons in the arcuate nucleus of female C57BL/6J mice. 761 32

beta-Endorphin (beta-endo) (1-31) is the active opioid peptide product of pro-opiomelanocortin processing. Further post-translational modifications of beta-endo(1-31) yield beta-endo(1-27), (1-26) and their acetylated forms which are considered to be opiate receptor antagonists. Mechanistically, alteration in opiatergic properties is likely to result in the loss of a number of physiological functions including reproductive capacity. The purpose of this study was to determine whether there are changes in the way beta-endo neurones process the peptide with age in female C57BL/6J mice. Pooled extracts of arcuate nucleus (ARC) and preoptic area (POA) of 3- to 4-month-old normally cycling (4-5 days at dioestrus), 12- to 13-month-old irregularly cycling (5-7 days at dioestrus), 23- to 24-month-old acyclic (in persistent dioestrus) animals were subjected to reversed-phase HPLC (n = 4 experiments). Column fractions were assayed for beta-endo-like-immunoreactivity by sequence-specific RIAs. The opiate receptor active as well as opiate receptor antagonist forms of beta-endo were present in both ARC and POA at all three age groups although their ratios varied. beta-Endo(1-31), the active opiate, was the predominant form in young animals. At middle age there was a threefold (P < 0.05, ANOVA) increase in the antagonist forms of beta-endo and this was associated with a significant (P < 0.05, ANOVA) increase in the ratio of antagonist to active forms. This was accompanied by a trend toward an increase in acetylated forms of beta-endo in middle-aged mice. HPLC profiles from hypothalami of old animals more closely resembled those of young females. The increase in the antagonist forms of beta-endo at middle age may contribute to a decline of opiatergic influences in the female C57BL/6J mouse and suggest a mechanism whereby alterations in opiate influence over gonadotrophin control may occur.
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PMID:Hypothalamic processing of beta-endorphin in female C57BL/6J mice is altered at middle age. 773 64

The effects of short-term phenobarbital administration were evaluated in 6 adult mixed-breed dogs that received phenobarbital (5 mg/kg of body weight, PO, q 12 h) for 8 consecutive weeks. Six additional dogs served as untreated controls. At 2-week intervals, endogenous adrenocorticotropic hormone (ACTH) concentration and cortisol concentration before and 2 hours after administration of porcine aqueous ACTH (2.2 IU/kg, IM) were measured. By means of one-way ANOVA, we were not able to detect a significant (P > or = 0.05) difference in endogenous ACTH concentration and cortisol concentration before and after exogenous ACTH administration within groups over time or between groups at any time. To evaluate effects of long-term phenobarbital administration, sera and plasma were collected from 5 epileptic dogs that had received phenobarbital for > 2 years and had serum phenobarbital concentrations > 20 micrograms/dl. Endogenous ACTH concentration and cortisol concentration, before and after administration of ACTH, were within established reference ranges for all 5 dogs. Together, these results suggest that phenobarbital administration alone does not affect endogenous ACTH concentration or response to exogenous ACTH administration in dogs, and that these may be valid screening tests for hyperadrenocorticism in most dogs receiving phenobarbital.
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PMID:Effects of short- and long-term administration of phenobarbital on endogenous ACTH concentration and results of ACTH stimulation tests in dogs. 792 10


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