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)

We evaluated the presence of anterior pituitary hormones; follicle-stimulating hormone (FSH) and its beta-subunit (beta-FSH), luteinizing hormone (LH) and its beta-subunit (beta-LH), beta-subunit of thyroid-stimulating hormone (beta-TSH), adrenocorticotropic hormone (ACTH), growth hormone (GH), and prolactin (PRL); the placental hormone human chorionic gonadotropin (hCG); and somatostatin, in paraffin and frozen sections of the human thymus. Epithelial cells in the medulla were immunoreactive for most of these hormones, in varying density and intensity of labeling. The cells labeled varied from epithelial cells surrounding Hassall's corpuscles toward solitary cells or small epithelial aggregates in the medulla. FSH immunoreactivity did occur predominantly in epithelial cells of the cortex, in apparent contrast to the predominant medullary location of cells immunolabeled for beta-FSH. The epithelial nature of FSH-immunoreactive cells was confirmed by two-color immunohistochemistry with anti-keratin antibody. In addition to FSH, some epithelial cells in subcapsule and cortex were labeled by antibodies to beta-FSH, beta-LH, beta-TSH, ACTH, GH, and PRL. Some macrophage-like cells surrounded by a rosette of lymphocytes were immunoreactive for FSH and GH. Some interdigitating reticulum-like cells were labeled by anti-beta-LH. Immunolabeling of lymphocytes was found for hCG, especially lymphocytes in the medulla. Two-color immunohistochemistry with anti-CD3 revealed a strong CD3 expression on hCG-immunoreactive cells, whereas CD3-negative cells were hCG-negative. T cells immunolabeled for hCG were also found in peripheral lymphoid organs.
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PMID:The neural and neuro-endocrine component of the human thymus. II. Hormone immunoreactivity. 139

The effects of intravenous human atrial natriuretic factor ANF(99-126) administration on anterior pituitary hormone secretion have not been extensively investigated in humans. We repeatedly studied 10 healthy volunteers (5 female, 5 male, aged 28 +/- 2 years) on 2 occasions, 3 days apart. In randomized, single blind order, subjects received pretreatment with either placebo or intravenous ANF(99-126) (bolus 100 micrograms/kg, 30-min infusion of 0.1 micrograms/kg.min). Subsequently on both occasions subjects received a combined intravenous bolus injection of pituitary releasing hormones (200 micrograms thyrotropin releasing hormone, 100 micrograms gonadotropin releasing hormone and 100 micrograms human adrenocorticotropin releasing hormone; Bissendorf, Hannover, FRG). Plasma concentrations of adrenocorticotropic hormone (ACTH), cortisol, luteinizing hormone (LH), follicle-stimulating hormone (FSH), growth hormone (GH), thyrotropin (TSH), prolactin, ANF and cyclic guanosine monophosphate (GMP) were determined by radioimmunoassay. ANF(99-126) treatment induced a significant reduction in basal ACTH plasma concentrations and tended to decrease basal plasma cortisol. The TSH response to combined releasing hormone administration was significantly diminished after ANF(99-126) pretreatment. In women, the releasing hormone induced prolactin increase was reduced after ANF(99-126) pretreatment. With the present study design, ANF(99-126) did not alter the basal or releasing hormone stimulated plasma concentrations of cortisol, LH, FSH and GH. Releasing hormone administration did not affect ANF and cyclic GMP plasma levels. In humans, effects of natriuretic peptides on anterior pituitary hormone secretion may have to be considered with investigational or therapeutic administration of ANF analogues or agents interfering with the ANF metabolism.
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PMID:Effects of atrial natriuretic factor on anterior pituitary hormone secretion in normal man. 139 23

In a previous study, we showed that the local administration of melatonin in the mediobasal hypothalamus (MBH), but not the preoptic area (POA), caused a premature increase in the secretion of FSH and growth of the testes in sexually inactive Soay rams exposed to long days. To extend these observations, we have now measured blood concentrations of prolactin and beta-endorphin and the associated peripheral responses in the same animals, to establish whether the treatments produced multiple endocrine changes such as those which occur following exposure to short days. Groups of rams were initially exposed to alternating 16 weekly periods of long days (16 h light: 8 h darkness; 16L:8D) and short days (8L:16D) for at least 9 months to entrain the seasonal cycles in the secretion of the pituitary hormones. The treatments were started at 10 weeks under long days, when the animals had a physiology characteristic of the early summer with high blood plasma concentrations of prolactin (associated with growth of the summer pelage), and low concentrations of beta-endorphin (associated with low body weight). The animals were assigned at random to the following treatments: (i) micro-implants of melatonin in the MBH, (ii) microimplants of melatonin in the POA, (iii) empty implants in the MBH or POA to act as operated controls, and (iv) no surgery to act as unoperated controls (n = 12 rams/treatment). The micro-implants consisted of 22-gauge stainless-steel needles with melatonin fused inside the tip. The implants were inserted bilaterally in the brain, and left in place for 12-14 weeks. The observations continued for a total of 28 weeks while the animals remained under long days. The administration of melatonin in the MBH induced a rapid decreased in plasma concentrations of prolactin while in the POA it induced a less marked but significant effect. The mean times to minimum concentrations of prolactin were 7.4 +/- 0.4, 17.3 +/- 2.8 and 26.0 +/- 0.3 weeks for the MBH, POA and combined control groups respectively (MBH vs control, P < 0.001, POA vs control P < 0.01). In the MBH group, the concentrations of prolactin subsequently increased to a maximum 6 weeks after the end of melatonin treatment. The changes in prolactin were accompanied by changes in growth and moulting of the pelage; only animals in the MBH group showed a conspicuous moult associated with the change from low to high prolactin secretion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of placing micro-implants of melatonin in the mediobasal hypothalamus and preoptic area on the secretion of prolactin and beta-endorphin in rams. 140 51

Endogenous opioid peptides (EOPs) stimulate prolactin (PRL) release in various physiological conditions in the rat. Moreover, EOPs are essential in initiating and maintaining the nocturnal PRL surges that occur over the first half of gestation in the rat. The purpose of this study was to investigate the potential role of the opioid beta-endorphin (beta-End) in mediating the nocturnal PRL surges. Day 8 pregnant rats received an infusion of 2.5, 10, 25 or 100 ng/microliters/min beta-End intracerebroventricularly (i.c.v.) for 15 min at 12.00 h, an intersurge period. PRL increased in a dose-dependent manner and from this, the largest dose was used in subsequent experiments to ensure maximal opioid receptor stimulation. The next experiment defined the temporal sensitivity of the neuroendocrine system regulating PRL surges to exogenous beta-End. Day 8 pregnant rats showed dramatic PRL responses to beta-End when given at midnight (presurge) or 12.00 h (intersurge), but greatly attenuated responses at 02.00 h (early surge) and 04.00 h (late surge). Animals treated at 06.00 h (postsurge) showed recovered responsiveness to beta-End. To determine what may account for the significantly lower PRL increases to beta-End during the surge, day 8 pregnant rats received 100 mg/microliters/min beta-End i.c.v. for 15 min at 10.00 h, and then again at 12.00 h. All animals showed PRL increases greater than 1,140 ng/ml at 10.00 h, but the subsequent response to beta-End at 12.00 h was reduced by 70%. In another experiment, beta-End was infused at midnight and the animals were monitored for a subsequent endogenous nocturnal PRL surge.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Time-dependent changes in beta-endorphin-stimulated prolactin release during pregnancy. 140 79

Since it has become possible to sample hypophysial portal blood from sheep without totally compromising pituitary function, several important features of the secretion of hypothalamic hormones have been elucidated. The secretion of gonadotropin-releasing hormone (GnRH) has been detailed most thoroughly with the important observation that each pulsatile discharge of luteinizing hormone (LH) is the direct result of a large secretory episode of GnRH from the hypothalamus. There is high fidelity in the GnRH relationship in terms of frequency and amplitude. During the LH surge, additional factors such as an alteration in the degree of enzymic degradation of GnRH may be important physiological mechanisms. The secretion of factors that control the release of growth hormone (GH), prolactin and adrenocorticotropic hormone (ACTH) have also been studied. Hypothalamic factors controlling GH and ACTH release do not bear such an explicit relationship to the secretory episodes of pituitary hormone as seen with the GnRH/LH axis. The factor involved in the acute stress-induced release of prolactin has not yet been identified in sheep.
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PMID:What can we learn from sampling hypophysial portal blood? 142 30

Milk flow in nine primiparous cows with disturbed milk ejection (D) and in six corresponding control animals (C) with normal milk removal was recorded during machine milking and blood samples were taken before and during milking to determine plasma oxytocin, vasopressin, prolactin, cortisol, oestradiol-17 beta, luteinizing hormone, progesterone and beta-endorphin concentrations. Manual teat stimulation before milking lasted for 1 min. After milk flow had stopped, air was blown into the vagina for 2 min. When milk flow had stopped again, 1 i.u. oxytocin and finally 10 i.u. oxytocin were injected to remove residual milk. During and after teat stimulation, oxytocin remained basal in D, but increased in C, whereas prolactin increased in both groups. While 94% of total milk was obtained in C during this period, only 9% could be removed from D, indicating lack of alveolar milk ejection. During vaginal stimulation, oxytocin increased transiently in D and more than by teat stimulation in C. This allowed the removal of 75% of milk in D, whereas almost no more milk was available in C. After oxytocin injections, 3 and 16% of residual milk were obtained in C and D respectively. Basal oestradiol-17 beta concentration was higher in D than in C (11.6 and 2.0 ng/l respectively), whereas beta-endorphin level was lower (24.1 and 86.6 micrograms/l respectively). Basal concentration of luteinizing hormone and progesterone, and concentration of cortisol and vasopressin before and during milking were comparable in C and D. We conclude that in cows with disturbed milk ejection afferent nervous pathways to the hypothalamus were intact, because prolactin was released by teat stimulation. However, oxytocin was only released by vaginal stimulation, i.e. milk ejection was centrally inhibited during teat stimulation.
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PMID:Aetiology of disturbed milk ejection in parturient primiparous cows. 145 33

Neuroendocrine dysfunctions, in part similar to those found in depression, are present in chronic alcoholism. The aim of this investigation was to evaluate the effects of chronic alcohol intake on cortisol secretion in basal conditions, after dexamethasone (DXT) suppression or corticotropin (ACTH) stimulation in 10 alcoholic men, during active drinking and after two weeks of alcohol withdrawal. The 24-hour, day- and night-time urinary cortisol and melatonin levels, and the effects of thyrotropin releasing hormone (TRH) on thyrotropin (TSH) and prolactin (PRL) secretions were studied in the same subjects. The data were correlated to the scores obtained by the Hamilton Rating Scale for depression and compared to those found in healthy subjects. Increased cortisol levels and the lack of DXT suppression of cortisol secretion are considered to be alcohol-dependent inasmuch as they disappear in most patients after alcohol withdrawal. The cortisol response to ACTH 1-24 infusion measured before and after alcohol withdrawal was similar in the patients we studied; moreover no significant difference was found between patients and controls. The increment of urine free cortisol levels in active alcoholics was not statistically significant. Urine cortisol levels became similar to those of the control subjects after alcohol withdrawal. The increased diurnal values of urine melatonin and the inversion of the physiological ratio between nocturnal and diurnal levels observed during alcohol intake became normal upon alcohol withdrawal. The TSH and PRL responses after the administration of 50 or 200 micrograms TRH were higher in alcoholics than in controls, while a blunted response is known to occur in depression.
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PMID:[The neuroendocrine aspects of chronic alcoholism: the effect of alcohol intake and its withdrawal]. 146 29

It is well known that the opiate peptides, especially the pro-opiomelanocortin (POMC)-related peptide beta-endorphin, stimulate the release of prolactin (PRL) in the rat. In order to evaluate the involvement of PRL on the activity of POMC neurons in the arcuate nucleus, we have studied the effects of the injection of PRL into the third ventricle of intact and hypophysectomized rats as well as the effects of hyperprolactinemia induced by pituitary implants under the kidney capsule on POMC gene expression. The amounts of POMC mRNA in the arcuate nucleus were measured by in situ hybridization using a [35S]-labelled cDNA probe encoding for POMC. Hypophysectomy performed 2 weeks previously decreased by 24% the number of silver grains/unit of surface of labelled neurons. Intracerebroventricular injection of 3 micrograms of PRL 4 h before sacrifice induced a significant decrease in the hybridization signal of 32 and 20% in the intact and hypophysectomized rat, respectively. Hyperprolactinemia achieved by pituitary implants also led to a significant decrease in POMC mRNA levels. The present data show that hypophysectomy depresses hypothalamic POMC mRNA levels and that this effect is not related to the suppression of PRL secretion since this hormone exerts an inhibitory action on POMC gene expression. They suggest that the regulation of PRL secretion by short loop feedback mechanism might be well mediated by beta-endorphin which has already been shown to inhibit dopaminergic neuron activity in the arcuate nucleus.
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PMID:Prolactin regulation of pro-opiomelanocortin gene expression in the arcuate nucleus of the rat hypothalamus. 147 14

In order to test the hypothesis that the anorectic effects of D-fenfluramine involve mediation by increased serotonin (5-HT) activity we examined the effects of acute and chronic D-fenfluramine on the hypothalamic activities of 5-HT as well as the other major monoamine neurotransmitters noradrenaline (NA) and dopamine (DA). Precise and specific gas chromatograph/mass spectrometer analyses of NA, 5-HT and DA and their primary metabolites dihydroxphenylethyleneglycol (DHPG), 5-hydroxyindolacetic acid (5-HIAA) and dihydroxyphenylacetic acid (DOPAC), respectively, were made in combination with analysis of the hormonal correlates of the monoamines, glucose and adrenocorticotropin for NA, thyroid-stimulating hormone for 5-HT and prolactin for DA. Acute D-fenfluramine increased NA, while reducing 5-HT, functional activity. Chronic and acute after chronic, D-fenfluramine decreased both NA and 5-HT functional activity. The effect of acute D-fenfluramine on the DA system is consistent with a post-synaptic blockade which is compensated for by chronic treatment. Since chronic D-fenfluramine acted to depress noradrenergic tone, a further study was undertaken which showed that chronic D-fenfluramine does not impair the ability noradrenergic/sympathetic system to respond to stress. The results indicate that D-fenfluramine may not exert its anorectic and weight loss effects via serotonergic agonism and involvement of the NA and/or DA systems is likely.
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PMID:D-fenfluramine effects on hypothalamic monoamine activities and their hormonal correlates. 147 36

Both direct pituitary and indirect CNS mechanisms have been postulated for the influence of opiate agonists on prolactin secretion. By examining the interactions between terminals of neurons containing opioid peptides and hypothalamic TH-positive cell bodies, this paper addressed the anatomical basis for the latter mechanism. Initial electron microscopic studies directly demonstrated contact between opioid peptide terminals and dopaminergic cell bodies and provided some visual criteria for assessing opioid-dopamine interactions at the light microscopic level. Using these guidelines, we examined the rates of contact on both A12 and A14 neurons of each of the three opioid peptide families: pro-enkephalin, pro-dynorphin, and pro-opiomelanocortin (POMC). For A14 neurons, many of which project to the posterior pituitary, contact rates were estimated at 15, 20, and 5% for dynorphin, Met-enkephalin, and ACTH (a POMC derivative), respectively. In contrast, the A12 dopamine neurons, which regulate prolactin secretion by inhibition, showed a roughly 70% contact rate with dynorphin axons (P less than 0.001) with Met-enkephalin and ACTH contact rates remaining low at 20 and 5% respectively. Contact frequency varied significantly during the estrus cycle only with dynorphin contacts on A12 neurons. Proestrus and diestrus (less so) showed a small but significant (P less than 0.05) elevation in contact rates versus estrus, male, lactating and pregnant groups. No other significant difference emerged among these groups. On the basis of these observations, we conclude that dynorphin represents a significant and specific factor in the innervation of A12 dopamine neurons. This relationship may account for some if not most of the influence of opiate agonists and antagonists on prolactin secretion.
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PMID:Interaction of opioid peptide-containing terminals with dopaminergic perikarya in the rat hypothalamus. 149 60


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