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)

Corticotropin-releasing factor (CRF) injected into the cerebral ventricles of small mammals induces EEG limbic seizures, behavioral excitability, stereotyped behavior, and tardive enhancement of hippocampal theta voltage and frequency. Because we addressed this phenomenon when we explained the pathogenesis of infantile spasms in children, we wished to study the interference exerted by some gamma-endorphin fragments on EEG epileptiform and behavioral symptoms induced by CRF in the rabbit. Animals were implanted intracerebroventricularly (i.c.v.) with semichronic cortical and hippocampal electrodes, together with a cannula into the left lateral ventricle. When some gamma-endorphin derivatives (DT gamma E, DE gamma E) were injected intravenously (i.v.) for 4 days (or hydrocortisone once), they prevented the EEG ictal seizures induced in the hippocampus of rabbits by CRF injected i.c.v. Hydrocortisone and DE gamma E also prevented the appearance of scattered spiking and partially prevented tardive enhancement of theta voltage in the hippocampal EEG. Finally, DE gamma E also prevented stereotyped behavior and excitability induced by CRF. These results confirm the regulatory role exerted by CRF in limbic structure excitability and suggest that the above peptides may be involved in a regulatory feedback mechanism of CRF metabolism or activity. The possibility that these peptides may also have interesting antiepileptogenic properties should be considered.
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PMID:Some endorphin derivatives and hydrocortisone prevent EEG limbic seizures induced by corticotropin-releasing factor in rabbits. 170 Sep 51

This study tested the role of melatonin in the regulation of seasonal physiological change in the pony stallion. Four 3-year-old, Welsh Mountain pony stallions were housed initially under the prevailing short-day photoperiod in December (8 of light [L]:16 h of darkness [D]) before being transferred to long days (16L:8D) on 13 January for the remaining 22 weeks of the study. On Day 76 (11 weeks later) the stallions began an 11-week period of daily melatonin treatment (20 mg orally, 8 h after lights on). Marked changes in mean plasma testosterone, beta-endorphin and cortisol concentrations occurred in response to long days and to subsequent melatonin treatment. Photostimulation produced a sharp rise in overall mean daily testosterone to a peak of 6.74 nmol/litre by Day 30. Values then fell to a nadir (3.17 nmol/litre) by Day 85, suggesting a role for melatonin in the termination of breeding activity in the horse. Cortisol and beta-endorphin values remained low throughout the first 11 weeks, but by Day 105 (Day 30 of melatonin treatment) concentrations had risen sharply, attaining a peak on Day 125 (510 pg beta-endorphin/ml, 50 ng cortisol/ml). Concentrations of both hormones had fallen by Day 77 of melatonin treatment (Day 152), perhaps as a result of refractoriness. Parallelism between beta-endorphin and cortisol suggests a pituitary origin for peripheral beta-endorphin. Diurnal variation in cortisol was observed under long days but no change in beta-endorphin was detected. Long days and melatonin treatment stimulated shedding of the winter and summer coats respectively, whereas growth rate was increased (2.03 kg/week) during the period of melatonin treatment relative to that of long days only (0.37 kg/week). The study provides evidence that the diurnal pattern of melatonin secretion mediates the reproductive and non-sexual responses to photoperiodic change in pony stallions.
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PMID:Effect of oral melatonin treatment on the seasonal physiology of pony stallions. 179 54

A 62-year-old man was admitted because of nausea and vomiting. Severe hyponatremia with renal sodium loss was found. Endocrinological studies revealed that the patient had isolated adrenocorticotropin (ACTH) deficiency and secondary adrenocortical insufficiency. Furthermore, an inappropriate secretion of antidiuretic hormone (ADH) in relation to the low plasma osmolality was observed at an early stage of hyponatremia. Hydrocortisone therapy effectively corrected his hyponatremia. Following the correction of hyponatremia, the value of free water clearance increased and the level of the plasma ADH decreased. Thus, the present case indicates that ACTH deficiency can cause the syndrome of inappropriate secretion of ADH.
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PMID:Inappropriate secretion of antidiuretic hormone in isolated adrenocorticotropin deficiency. 185 May 79

We have followed the hormonal response to exercise in twelve normal males cycling at a constant moderate load for ten minutes. Plasma concentrations of a variety of hormones were measured at set times before and during exercise and for twenty minutes afterward. The plasma concentration of norepinephrine and epinephrine and plasma activity of renin rose to a maximum at the end of exercise and then declined. The plasma concentrations of neurotensin and atrial natriuretic peptide followed a similar course. Plasma vasopressin rose to a peak at the end of exercise and then fell transiently below the initial value ten minutes after exercise. The plasma concentrations of aldosterone, prolactin and adrenocorticotropin increased during exercise but continued to do so, reaching a peak at ten minutes after exercise. Plasma growth hormone increased during exercise and continued to increase throughout the period of twenty minutes' recovery. Cortisol did not change during exercise but rose progressively during the recovery period. Plasma concentrations of glucagon did not change while that of insulin decreased during exercise. The plasma concentration of bombesin slowly increased during exercise and declined during recovery, reaching a basal value 10 minutes later.
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PMID:Temporal relations of the endocrine response to exercise. 187 87

Baseline 8 a.m. adrenocorticotropic hormone (ACTH) and cortisol levels and the postdexamethasone ACTH/cortisol values at 8 a.m. and 4 p.m. were determined in 86 depressed females diagnosed using DSM-III criteria. Postdexamethasone ACTH and cortisol values were significantly correlated with their baseline levels. We have shown that regression analysis should be used to assess dexamethasone-induced changes as the residual ACTH and cortisol responses, with the relative effects of the baseline data on the hormone responses being partialed out. The residual ACTH and cortisol values were significantly increased in the most severely depressed females as compared to minor depressives. The residual ACTH responses were markedly correlated with the residual cortisol responses. Cortisol nonsuppression during a depressive episode appeared to be determined by an augmented ACTH escape from dexamethasone suppression. The residual ACTH and cortisol responses could prove to be the most sensitive reflection of the disorder in the negative feedback by dexamethasone on the pituitary. In clinical practice, the ratio ln (postdexamethasone ACTH): ln (basal ACTH) can be used, since this ratio is linearly correlated with the residual ACTH responses.
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PMID:A revised interpretation of postdexamethasone ACTH and cortisol findings in unipolar depressed females. 196 60

1. Adrenal responses to intra-aortic infusions of pure synthetic ovine corticotrophin-releasing factor (CRF) have been investigated in functionally hypophysectomized calves previously fitted with an adrenal clamp. 2. CRF caused an increase in the output of cortisol from the adrenal gland, which was dose related over the range 4-8 pmol min-1 and maximal at the higher of these doses; this response was observed at a dose below that which produced any change in adrenal vascular resistance. Cortisol output was also found to be related linearly to the rate at which CRF was estimated to be presented to the gland during these infusions. 3. The infusions of CRF also provoked the release of small, but readily detectable, amounts of adrenocorticotrophin-like peptides (ACTH) from the gland. This was mainly in the form of ACTH1-39 with some pro-opiomelanocortin (POMC) also being released. 4. Comparison of the adrenal steroidogenic response to exogenous CRF with that to synthetic ACTH1-24 showed that CRF was the more potent; in each case cortisol output was related linearly to the presentation rate of the peptide. 5. It is concluded that the adrenal cortex in the calf is capable of releasing cortisol in response to exogenous CRF at low concentrations and is even more sensitive to CRF than it is to exogenous ACTH over the dose range that was employed.
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PMID:Adrenal responses to corticotrophin-releasing factor in conscious hypophysectomized calves. 196 66

It was previously shown in this laboratory that high affinity binding of [125I]ACTH-(1-24) to membranes from rat brain was inhibited by vasoactive intestinal polypeptide (VIP), GH-releasing factor (GRF), and dynorphin (DYN), but not by other peptides tested. We now show that these peptides compete for [125I]VIP binding in brain and for [125I]ACTH-(1-24) binding in adrenal cortex and promote steroidogenesis. The high affinity sites for [125I]ACTH-(1-24) in the rat brain and bovine adrenal had Kd values of 0.51 +/- 0.41 and 3.9 +/- 1.3 nM, respectively; and the Ki values for VIP were 5.4 +/- 4.2 and 1.4 +/- 0.51 nM, respectively. In rat brain and bovine adrenal the high affinity site for [125I]VIP had Kd values of 2.9 +/- 1.7 and 0.5 +/- 0.8 nM, respectively, and Ki values for ACTH of 23.6 +/- 14.0 and 22.2 +/- 33.0 nM, respectively. In brain, DYN and GRF inhibited binding of [125I]VIP with Ki values of 49 and 30 nM, respectively. Cortisol secretion from isolated bovine adrenal cortical cells was significantly stimulated by 10(-10) M ACTH, VIP, DYN, or GRF, and a maximal response occurred for each at 10(-8) M. However, maximal cortisol production in response to VIP, DYN, or GRF was only about half that by ACTH-(1-24). The combination of ACTH-(1-24) and VIP, each at 10(-10) M, was additive in stimulating cortisol production, whereas each at 10(-8) M caused no greater response than ACTH alone. There was an additive steroidogenic effect of VIP plus ACTH-(1-10), but not VIP plus ACTH-(11-24). Specific binding of [125I]ACTH-(11-24) in adrenal membranes was inhibited by unlabeled ACTH-(11-24), ACTH-(1-24), VIP, GRF, and DYN, but not by ACTH-(1-10), peptide T, TRH, alpha MSH, or beta-endorphin; there was no specific binding of [125I]ACTH-(1-10). Functional studies and binding data, in conjunction with the existence of homologous amino acid sequences, indicate that VIP, GRF, and DYN interact at a subpopulation of ACTH receptors that recognizes a moiety within the 11-24 sequence of the ACTH molecule.
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PMID:Adrenocorticotropin, vasoactive intestinal polypeptide, growth hormone-releasing factor, and dynorphin compete for common receptors in brain and adrenal. 196 78

The relationships between mood change, obstetric experience and alterations in plasma cortisol, beta-endorphin (beta-EP) and corticotrophin-releasing hormone (CRH) were examined in a prospective study of 97 primiparous Australian women. Psychological measures were administered between the 28th week of pregnancy and the 3rd postnatal month, including the Profile of Mood States (POMS) and the Montgomery Asberg Depressive Rating Scale (MADRS). Blood samples were collected for cortisol, beta-EP and CRH assay on most of these occasions and during labour. Factor analysis was used to identify key subsets of psychological variables for use in the subsequent analyses. 'Mood disturbance' and 'tiredness' factors peaked at 38 weeks' gestation, while 'difficulty falling asleep' was greatest around the time of birth. Cortisol, beta-EP and CRH concentrations rose significantly as pregnancy advanced and peaked at birth; plasma CRH correlated with plasma cortisol (r = 0.54) and beta-EP (r = 0.32). Women with the highest 'mood disturbance' and MADRS depression scores at 28 weeks' gestation received significantly more pain relief during labour. Those women whose mood deteriorated from 38 weeks' gestation to postnatal day 2 had larger falls in plasma beta-EP after delivery (p less than 0.01) than those women whose mood improved or remained constant. Women in this mood-deteriorated subgroup also had significantly higher MADRS depression scores at 3 months (p less than 0.01). Mild antenatal depression (MADRS greater than 13) occurred in 5.2% of women and mild postnatal depression in 4.7%. Overall, these data suggest a role for circulating CRH in the regulation of maternal cortisol secretion and significant relationships between maternal postnatal mood states and beta-EP and between antenatal mood states and obstetric events.
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PMID:Mood changes, obstetric experience and alterations in plasma cortisol, beta-endorphin and corticotrophin releasing hormone during pregnancy and the puerperium. 213 27

Neuroendocrine and sympathoadrenal responses to exhaustive graded treadmill exercise were examined in 17 male subjects of varying degrees of fitness. The mean duration of exercise to exhaustion was 15.2 +/- 0.7 (+/- SE) min. Exercise duration was inversely correlated with baseline heart rate (P less than 0.05). Compared to standing baseline values, mean plasma norepinephrine and epinephrine levels increased 339% and 301%, respectively, in an integrated 2-min blood sample collected immediately after completion of exercise. Mean adrenocorticotrophic hormone (ACTH), beta-endorphin (beta-EP), beta-lipotropin (beta-LPH), and prolactin levels increased 282%, 720%, 372%, and 211%, respectively, in an integrated 4-min blood sample beginning 2 min after completion of exercise. Cortisol levels increased 183% in the sample collected 17-21 min after exercise. The magnitude of these neuroendocrine responses to exercise was similar among individuals at the same relative intensity of exhaustive exercise, regardless of the duration of exercise. The exercise-induced increases of the pro-opiomelanocortin (POMC)-derived peptides, ACTH, beta-EP, and beta-LPH, were highly correlated with each other (P values less than 0.001), and were correlated with prolactin increases, (P values less than 0.05). During a 20-min recovery period after exercise, changes in heart rate, ACTH, and beta-LPH levels were correlated with duration of exercise, (P less than 0.01, P less than 0.03, and P less than 0.03, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of fitness on neuroendocrine responses to exhaustive treadmill exercise. 215 74

Suppression of endogenous cortisol production was assessed by a corticotropin-releasing hormone (CRH) test 24 hours after the last dose of the glucocorticoid in 48 patients (27 women and 21 men; mean age 48.9 [21-69] years) who had been taking fluocortolone for inflammatory rheumatic disease. Both during a few weeks of treatment (9 patients) and after a year (39 patients) complete suppression of endogenous cortisol production occurred in 17 patients, partial suppression in 17. This suppression did not unequivocally correlate with the dosage or duration of treatment, but there was a tendency towards it at higher dose levels (15-30 mg). Cortisol response to the CRH test was unremarkable in 14 patients. These results suggest that secondary adrenal insufficiency is to a considerable extent dependent on individual factors. Correspondingly the degree of suppression of the adrenal axis cannot be predicted for an individual patient without suitable testing.
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PMID:[Corticotropin-releasing hormone (CRH) test for monitoring glucocorticoid therapy]. 216 99


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