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)

Rat anterior pituitary quarters or acutely dispersed rat anterior pituitary cells were incubated in vitro, and the release of dynorphin A1-13-like immunoreactivity (Dyn A1-13-IR) into the incubation medium was studied. Addition of LHRH led to a concentration-dependent enhancement of the release of Dyn A1-13-IR with a maximum secretory rate which was about 4-fold higher than basal secretion. Dyn A1-13-IR was released by LHRH concomitantly with LH and FSH, and the concentration-response relationships as well as the time course were virtually identical. Gel filtration and HPLC revealed a single peak of Dyn A1-13-IR, with an apparent mol wt of about 6000. In addition to Dyn A1-13-IR, alpha-neo-endorphin-like immunoreactivity was released by LHRH. The LHRH-stimulated release of Dyn A1-13-IR was mimicked by the LHRH analog D-Ala6,des-Gly10-LHRH ethylamide and blocked in a competitive manner by the LHRH antagonist D-pGlu1,D-Phe2,D-Trp3,6-LHRH. Addition of TRH (5 microM), rat corticotropin-releasing factor (100 nM), arginine vasopressin (1 microM), or synthetic human pancreatic GH-releasing hormone (10 nM) produced no effect on Dyn A1-13-IR release. An extract of the rat medial basal hypothalamus stimulated the release of Dyn A1-13-IR and beta-endorphin-like immunoreactivity, and the former, but not the latter, effect was blocked by the LHRH antagonist D-pGlu1,D-Phe2,D-Trp3,6-LHRH. These results demonstrate that dynorphin-like material and other proenkephalin B-derived peptides are released concomitantly with LH and FSH from rat adenohypophysis in vitro upon activation of LHRH receptors. This may indicate that proenkephalin B-derived peptides coexist with LH and/or FSH in at least some gonadotrophs of the normal rat anterior pituitary gland.
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PMID:Corelease of dynorphin-like immunoreactivity, luteinizing hormone, and follicle-stimulating hormone from rat adenohypophysis in vitro. 286 8

LHRH has previously been found to be the only known hypothalamic releasing factor which can specifically stimulate the release of the opioid dynorphin and other proenkephalin B-derived peptides from the rat adenohypophysis in vitro. In the present study the mechanisms that regulate dynorphin release were further characterized. It was examined whether or not dynorphin release from the adenohypophysis in vitro is altered during inhibition of the secretion of various anterior pituitary hormones. Rat anterior pituitary quarters were incubated in vitro and hormone release into the incubation medium was measured by RIAs. Somatostatin, dopamine, T3, dexamethasone, and 5 alpha-dihydrotestosterone were used to inhibit the secretion of GH, PRL, TSH, ACTH/beta-endorphin, or LH/FSH, respectively. GH, PRL, or beta-endorphin release was inhibited without affecting the simultaneous release of dynorphin A-(1-13)-like immunoreactivity (Dyn A1-13-IR). Concentrations of T3, somatostatin, or dopamine which were effective in suppressing the evoked and/or basal release of TSH, GH, or PRL, respectively, produced no effect on Dyn A1-13-IR release caused by high potassium concentration (40 mM) or LHRH (500 pM). The LHRH-induced release of LH and FSH was inhibited by the glucocorticoid dexamethasone or the androgen 5 alpha-dihydrotestosterone. Under these conditions, Dyn A1-13-IR release was also reduced. However, whereas LH release was completely blocked by 5 alpha-dihydrotestosterone, FSH and Dyn A1-13-IR release was reduced only by 50%. The release of FSH and Dyn A1-13-IR in vitro from anterior pituitary glands taken from rats, castrated 3 weeks before, was enhanced to a similar extent (about 2.5-fold); the simultaneous enhancement of LH release was significantly (P less than 0.005) greater (about 5-fold). We conclude that the mechanisms which regulate the release and/or biosynthesis of dynorphin and other proenkephalin B-derived peptides of the adenohypophysis are similar to those of the gonadotropins but different from those of any other anterior pituitary hormone, and may be more closely related with FSH release than LH release. These data support the view that dynorphin of the normal rat adenohypophysis may be localized in at least a subpopulation of gonadotrophs.
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PMID:Release of dynorphin-like immunoreactivity from rat adenohypophysis in vitro during inhibition of anterior pituitary hormone secretion from individual cell types. 288 74

The present experiments assessed the involvement of endogenous opioids in the inhibition of FSH and LH release, ovulation and continuous sexual receptivity following exposure to constant illumination. In the first experiment, exposure to constant illumination resulted in persistent vaginal oestrus in all rats. The injection of naloxone resulted in marked elevations in serum FSH and LH, induced ovulation and increased the frequency of lordosis behaviour. It was concluded that endogenous opioid(s) participate in these effects. In Experiment 2, levels of beta-endorphin were found to be elevated in anterior pituitary and neurointermediate lobe tissue extracts from rats exposed to constant illumination, compared to levels in pro-oestrus rats. Naloxone injection into those rats exposed to constant illumination significantly increased hypothalamic levels of beta-endorphin compared to saline injected controls. This suggests that the blockade of opiate receptors increases beta-endorphin production, uptake and/or decreases its release from the hypothalamus. These results, and the known inhibitory action of beta-endorphin on LH release suggest that it may be this opioid, perhaps in conjunction with pineal products, which is responsible for the observed anti-reproductive effects of constant illumination.
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PMID:The role of endogenous opioid peptides in the effects of constant illumination on reproductive function in the rat. 293 50

Anomalous anterior pituitary hormone responses to acute administration of TRH and LRH have previously been observed in patients with primary affective disorders (PAD), with TRH eliciting GH, FSH and LH rises, and LRH eliciting GH and Prl rises. We examined whether the same unusual responses were present also for beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) in 15 PAD patients, in 9 patients with secondary affective disorders (SAD), and in 7 controls. TRH (500 micrograms iv) elicited rises of beta-EP plasma levels in 5 PAD and 2 SAD patients, and of beta-LPH in 4 PAD and 3 SAD patients. LRH (150 micrograms iv) elicited rises of plasma beta-EP levels in 2 PAD and 2 SAD patients, and of beta-LPH in 5 PAD and 2 SAD patients. No rises of beta-EP and beta-LPH plasma levels were observed in PAD patients after saline administration, nor in the controls after TRH, LRH or saline administration.
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PMID:Abnormal beta-endorphin and beta-lipotropin responses to TRH and LRH administration in primary and secondary affective disorders. 294 41

To probe the possible role of endogenous opiates in Sertoli cell proliferation during testicular development, the effect of interfering with beta-endorphin action either in vivo or in vitro was determined. The percent of Sertoli cells dividing was measured with quantitative autoradiography in [methyl 3H]-thymidine-exposed fetal testes maintained in organ culture with or without FSH, in the presence or absence of the opiate blocker naloxone. After 1 or 2 days in culture, naloxone enhanced the rise in Sertoli cell proliferation seen with FSH alone, while 2 days of incubation with naloxone alone markedly raised the percent of Sertoli cells dividing above that in untreated cultures. Moreover, when endorphin antiserum was injected directly into testes of pups and Sertoli cell proliferation in vivo measured 8 or 19 h later, there was a dramatic increase in the percent of Sertoli nuclei labeled by [methyl 3H]-thymidine compared to controls. These findings suggest that beta-endorphin produced within the testis is a paracrine modifier of the proliferative response of Sertoli cells to FSH. This implies that communication occurs between Leydig and Sertoli cells during development via endogenous testicular opiates.
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PMID:FSH-induced Sertoli cell proliferation in the developing rat is modified by beta-endorphin produced in the testis. 294 40

A newly established RIA was used to measure changes in the concentration of beta-endorphin in peripheral blood and pituitary tissue from adult Soay rams living outside under natural conditions and housed indoors under artificial photoperiods. A pronounced seasonal cycle in plasma beta-endorphin immunoreactivity occurred in the outdoor animals, with low levels in spring and early summer (February-May; less than 200 pg/ml plasma) and maximal levels 10-20 times higher in late summer and autumn (July-October). Seasonal changes in plasma levels of PRL, FSH, and cortisol, testis size, and body weight were also monitored; the seasonal cycle in the levels of immunoreactive beta-endorphin occurred in parallel with the cycle in plasma FSH and body weight. There were no significant seasonal changes in plasma cortisol concentrations. Marked changes in the plasma levels of beta-endorphin were also seen in rams kept under the artificial photoperiod regimen of alternating 12- to 16-week periods of long days (16 h of light and 8 h of darkness; 16L:8D) and short days (8L:16D). Transfer from long days to short days led to a greater than 20-fold increase in the levels of beta-endorphin, reaching a maximum after 4-8 weeks; the reverse switch in photoperiod led to a rapid decrease in the levels. There was no diurnal rhythm in the plasma levels of beta-endorphin based on hourly samples collected for 24 h under long and short days. The total content of immunoreactive beta-endorphin in the pituitary gland was lower in rams under short days than under long days, converse to the pattern in the blood. Sephadex chromatography of the plasma samples revealed that most of the beta-endorphin immunoreactivity coeluted with synthetic beta-endorphin-(1-31), and a small amount of activity eluted with beta-lipotropin. The seasonal and photoperiod-induced changes were largely due to changes in the levels of beta-endorphin. Extracts of pituitary tissue revealed a large proportion of beta-lipotropin to beta-endorphin compared to plasma, with no consistent change in ratio related to the photoperiod. The overall results illustrate that there are pronounced seasonal and photoperiod-induced changes in immunoreactive plasma beta-endorphin levels in the ram. Under artificial photoperiods, long days inhibit and short days stimulate beta-endorphin secretion. Under natural conditions, the development of refractoriness to both the inhibitory effects of long days and the stimulatory effects of short days may explain the timing of the annual cycle of beta-endorphin secretion.
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PMID:Beta-endorphin secretion in rams related to season and photoperiod. 294 17

This research was carried out to define the effects on men of head-out water immersion in a bath at 38.41 +/- 0.04 degrees C (mean +/- S.E.) with a method similar to that used for therapeutical rehabilitation and time of immersion of 30 minutes. Beta-endorphin, renin activity, aldosterone, cortisol, HGH, FSH, LH, TSH, T3, T4 and prolactin haematic levels were analysed. Seventeen healthy subjects (fourteen males and three females), aged 21-65 years (mean age 29.8 +/- 2.6) were studied. Water immersion caused a decrease in FSH and LH haematic concentrations; no significant changes occurred in beta-endorphin, renin activity, aldosterone, prolactin, cortisol, HGH, TSH, T3, T4 and FTI values. Thirty minutes after the end of immersion, FSH and LH levels returned to pre-immersion values. The probable pathogenesis of these observations is suggested.
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PMID:[Hormonal, beta-endorphin and renin activity changes in man during partial immersion, as a therapeutic method, in water at 38 degrees C]. 295 Mar 39

It is known that prolonged therapy with cytotoxic drugs may affect the endocrine system. The present study was carried out to establish whether administration of chemotherapeutic drugs acutely influences hypophyseal and pineal activities. Nineteen patients affected by solid tumors were included in the study, 5 of whom were treated with CMF, 4 with FEC, 4 with CEV, and 6 with CDDP. Cytotoxic drugs were intravenously administered. Venous blood samples were collected at zero time and at 30, 60, 120 and 180 min after drug administration. On a separate occasion, venous blood samples were drawn during a saline infusion only. In each sample FSH, LH, GH, PRL, TSH, cortisol, melatonin and beta-endorphin were determined by the RIA method. The only significant changes observed in this study were a rise in PRL and a decrease in beta-endorphin after CDDP administration. Melatonin was enhanced after CDDP and CMF, and cortisol decreased after CMF and FEC, but their variations were not statistically significant with respect to those seen during saline infusion.
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PMID:Acute effects of various chemotherapeutic combinations on hypophyseal and pineal hormone secretions in cancer patients. 295 96

Plasma beta-endorphin, prolactin (PRL), FSH and LH were measured in 17 volunteer male subjects at rest and under the stress caused by a long-distance nordic ski race. The race induced increased levels of beta-endorphin and PRL in all skiers. The changes in PRL with exercise were significantly related to the changes in beta-endorphin (r = 0.69, p less than 0.001). Furthermore, the highly trained skiers training over 150 km.week-1 of nordic ski showed consistently higher post-exercise beta-endorphin and PRL levels than the moderately trained skiers who trained for 20 km.week-1. In addition the race induced slight falls in FSH and LH; however plasma gonadotropin levels did not show any correlation with plasma beta-endorphin concentrations and did not differ between the two groups of skiers. These results suggest that endogenous opioid peptides may modulate PRL secretion in heavy exercise, since they are of minor importance in the release of FSH and LH in such a situation. The observations also suggest that the degree of previous training and the exercise intensity do seem to be responsible for the hormonal changes.
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PMID:Plasma levels of beta-endorphin, prolactin and gonadotropins in male athletes after an international nordic ski race. 296 35

Endogenous opioid peptides have been seen to play a role in regulating immunity and tumor growth. This study was carried out to investigate opioid activity in human cancer. We evaluated by radioimmunoassay beta-endorphin plasma levels on blood samples collected at 9.00 a.m. from 121 cancer patients and 42 healthy subjects. In 22 cancer patients and in 12 controls, beta-endorphin circadian rhythm was also investigated. Finally, in 14 cancer patients and in 10 controls GH, PRL, FSH, LH and cortisol serum levels were measured after the administration of a metenkephalin analogue, FK 33-824 (0.3 mg i.v.). No significant differences were seen in beta-endorphin mean levels between cancer patients and normal subjects. Moreover, no differences were found between patients with or without metastases, nor between those with or without chronic pain. beta-Endorphin circadian rhythm appeared to be altered in 16/22 cancer patients, and anomalous hormonal responses to FK 33-824 were seen in 13/14 patients. This study shows an altered opioid activity in human neoplasms, whose clinical significance remains to be determined.
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PMID:Alteration of opioid peptide circadian rhythm in cancer patients. 296 39


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