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)

Double-label immunocytochemistry was used to determine whether estradiol-induced progestin receptors and either beta-endorphin or leucine-enkephalin are colocalized in female guinea pig brain. Ovariectomized, adult guinea pigs were implanted with capsules containing estradiol-17 beta to induce high levels of progestin receptors, and injected intracerebroventricularly with colchicine to improve visualization of the opiate peptides. Sections through the hypothalamus and preoptic area were processed for progestin receptor, followed by beta-endorphin or leucine-enkephalin immunocytochemistry. As reported previously, high concentrations of progestin receptor-immunoreactive (PR-IR) cells were found in the preoptic area (medial and periventricular portions, medial preoptic nucleus) and hypothalamus (anterior hypothalamic and arcuate nuclei, ventrolateral area). Many beta-endorphin-IR cells contained PR-IR in the arcuate nucleus and its surroundings (33%) and in the dorsomedial area of the hypothalamus (64%). Scattered enkephalin-IR cells were found in the septal nucleus, medial and lateral preoptic area, bed nucleus of the stria terminalis, and the arcuate nucleus. The ventromedial nucleus of the hypothalamus and dorsolateral magnocellular nucleus, respectively, contained moderate and heavy concentrations of enkephalin-IR cells. Although some of these areas also contained PR-IR, enkephalin-IR was colocalized consistently with PR-IR only in a small number of cells in the arcuate nucleus and ventromedial/ventrolateral area of the hypothalamus. These data, taken together with earlier observations that virtually all cells containing estradiol-induced PR-IR also contain estrogen receptor-IR, provide neuroanatomical evidence that hypothalamic actions of progesterone and estradiol may be mediated by beta-endorphin and/or enkephalin.
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PMID:Immunocytochemical colocalization of progestin receptors and beta-endorphin or enkephalin in the hypothalamus of female guinea pigs. 214 16

Stress-related activation of the hypothalamic-pituitary-adrenal axis (HPA) is associated with suppression of the reproductive axis. This effect has been explained by findings indicating that corticotropin-releasing hormone suppresses hypothalamic gonadotropin-releasing hormone (GnRH) secretion via an opioid peptide-mediated mechanism, and that glucocorticoids suppress both GnRH and gonadotropin secretion and inhibit testosterone and estradiol production by the testis and ovary, respectively. To evaluate whether glucocorticoids suppress the effects of estradiol on its target tissues, we examined the ability of dexamethasone to inhibit estradiol-stimulated uterine and thymic growth in ovariectomized rats. Estradiol alone, given daily for 5 days, caused dose-dependent uterine and thymic growth. Dexamethasone alone, given daily for 5 days, caused a dose-dependent decrease in body weight gain and in thymic growth. When estradiol and dexamethasone were administered simultaneously, however, body weight gain and thymic growth were also inhibited (p less than 0.05). Dexamethasone decreased estradiol-induced uterine cytosolic and nuclear estrogen receptor concentrations (E2 R0, p less than 0.05; E2nR0, respectively), but had no effect on estradiol-induced progesterone receptor concentrations (P4R0, p greater than 0.05). Levels of uterine glucocorticoid receptors were not affected by estrogen and/or dexamethasone treatment. These findings suggest that stress levels of glucocorticoids, administered over a 5-day interval, block the estradiol-stimulated growth of female sex hormone target tissues. This effect may be partially mediated by a glucocorticoid-induced decrease of the estradiol receptor concentration. Thus, another mechanism by which the HPA may influence reproductive function during stress is by a direct effect of glucocorticoids on the target tissues of sex steroids.
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PMID:Glucocorticoids inhibit estradiol-mediated uterine growth: possible role of the uterine estradiol receptor. 231 Aug 19

Opioid peptides have a variety of actions on inter alia pituitary hormone secretion and the immune system. Release of endogenous opioids has been found to stimulate growth of experimental breast cancers and opiate receptor blockers have reduced the growth of chemically induced rat breast tumors. Opioid peptides may therefore play a role in human breast cancer. Invasive ductal carcinomas from 61 premenopausal women were immunocytochemically analyzed for the presence of opioid peptide immunoreactivity. Positive staining was unambiguously identified in 34 of the tumors (56%). In addition, a medullary carcinoma was positive. In a smaller series of tumors, opioid peptide immunoreactive cells were detected in both primary tumors and metastases. Positive tumor cells were usually few and scattered. Therefore, underestimates of their true frequency of occurrence are likely to have occurred, making accurate correlations with clinical behavior and estrogen receptor status difficult. No correlations with estrogen receptors were established for the unambiguously opioid peptide-positive tumors. Many of the positive tumors also stained with antibodies to gamma-endorphin and alpha-melanocyte-stimulating hormone, suggesting the presence of proopiomelanocortin-derived peptides in them. However, peptides derived from other opioid precursors also may be present in breast cancer.
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PMID:Immunoreactive opioid peptides in human breast cancer. 246 45

The aim of this study was to ascertain whether there is a correlation between gonadal steroids and opioid control of prolactin (PRL) secretion. Four castrated men, aged 18 to 24 years were submitted to intravenous injection of 250 ug of a met-enkephalin analog (D-Ala2-Mephe4-Met-(o)-ol-Enkephalin, FK 33824) (DAMME). In normal men DAMME injection was also performed on the 6th day after treatment with clomiphene citrate (CC) (200 mg/day for 5 days), a specific nonsteroidal estrogen receptor blocker. In castrated men and in normal men after CC treatment, there was a lower PRL response to DAMME than in controls (P less than 0.0005). These results suggest that gonadal steroid deficiency seems to cause a change in the opioid system and/or dopaminergic control of prolactin secretion.
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PMID:Gonadal steroids deficiency and prolactin response to a met-enkephalin analog in man. 401 22

A patient with clinical hypercortisolism and an infiltrating ductal carcinoma of the right mammary gland is presented. Provocative testing of adrenal function demonstrated the pattern of ectopic adrenocorticotropic hormone (ACTH) production. Ultrastructural analysis of the tumor revealed 150-200 nm electron-dense granules that when primarily fixed in OsO4 appeared as membrane-bound, centrally dense cored granules. ACTH was extracted from the tumor tissue and immunocytochemically localized in the tumor cell cytoplasm. A clinically significant level of estrogen receptor protein was present in the tumor tissue (120 fmol/mg protein). This case confirms the ability of mammary carcinoma to produce the ectopic ACTH syndrome.
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PMID:Adrenocorticotropin production by a mammary carcinoma. 626 28

The aim of this study was to ascertain whether there was an interrelationship between gonadal steroids and endogenous opioid peptides. The effects of naloxone (20 mg, intravenously) and of a met-enkephalin analog (DAMME) (250 micrograms, intravenously) on gonadotropin secretion in three castrated men (18 to 23 years of age) and in five age-matched normal men were studied. Normal subjects were studied before and after treatment with a specific nonsteroidal estrogen receptor antagonist, clomiphene. Naloxone caused a significant increase in luteinizing hormone (LH) (P less than 0.05); in these subjects, clomiphene treatment significantly increased LH and follicle-stimulating hormone plasma levels but totally suppressed the naloxone-induced rise in LH. In castrated men, naloxone failed to increase plasma LH levels. However, DAMME significantly reduced plasma LH levels in normal, in castrated, and in clomiphene-treated normal subjects. The results demonstrate that in castrated subjects who lack gonadal steroids and in normal subjects with blocked estrogen receptors there is a reduced opioid inhibitory tone on gonadotropin secretion. The effect of DAMME on gonadotropin secretion, however, is not influenced by the gonadal steroid environment.
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PMID:Gonadal steroids and opioid control of gonadotropin secretion in man. 631 69

The neural components underlying the influence of photoperiod upon reproductive functioning are poorly understood. In this study, we have used immunocytochemistry to examine whether changes in photoperiod may influence specific neuronal cell populations implicated in mediating gonadal steroid feedback actions on GnRH neurons. Short day (SD) exposed ewes in the midluteal stage of the estrous cycle and long day (LD) anestrous ewes were perfused in pairs and hypothalamic brain sections immunostained for tyrosine hydroxylase (TH), neuropeptide Y (NPY), beta-endorphin (betaE), and the estrogen receptor (ER). The number of ER-immunoreactive cells detected within the preoptic area, but not the hypothalamus, was approximately 20% higher (P < 0.05) in LD ewes compared with SD animals. The numbers of TH-immunoreactive neurons comprising the A12, A14, and A15 cell groups were not different between LD and SD ewes, and the percentage of A12 (approximately 15%) and A14 (approximately 25%) neurons expressing ERs was similarly unaffected by photoperiod. The number of betaE neurons detected in the arcuate nucleus was 50% lower (P < 0.05) in SD vs. LD ewes, whereas NPY-immunoreactive cell numbers in the median eminence were 300% higher (P < 0.05). Approximately 3% of NPY neurons in the median eminence, and 10% in the arcuate nucleus, expressed ER immunoreactivity in a photoperiod-independent manner. These studies indicate that changes in photoperiod may regulate ER expression within the preoptic area and suggest that hypothalamic NPY and betaE neurons are involved in the seasonal regulation of reproductive activity in the ewe.
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PMID:Effects of photoperiod on estrogen receptor, tyrosine hydroxylase, neuropeptide Y, and beta-endorphin immunoreactivity in the ewe hypothalamus. 916 52

Raloxifene is a selective estrogen receptor modulator with a benzothiophene structure, that exerts an estrogen-like action on some target tissues and an anti-estrogenic action on the uterus and breasts. A limited number of data are available on the effect of raloxifene on neuroendocrine function. Since beta-endorphin (beta-EP) is considered a marker of neuroendocrine function, the aim of the present study was to evaluate the effects of a 14 day treatment with a raloxifene analog, LY 117018, on beta-EP content in the hypothalamus, hippocampus, anterior and neuro-intermediate pituitary lobe, and in the plasma of fertile and ovariectomized (ovx) rats. The effect of LY 117018 in ovx rats was compared to that of 17 beta-estradiol. beta-EP contents were measured by a specific radioimmunoassay. While ovariectomy determined a significant decrease in beta-EP levels in the anterior and neurointermediate pituitary lobe and plasma (p < 0.01), no changes of beta-EP content in the hypothalamus and hippocampus were found. The administration of 17 beta-estradiol or LY 117018 in ovx rats significantly increased beta-EP concentration in the anterior and neurointermediate pituitary lobe, in the hypothalamus and plasma (p < 0.01), though they did not significantly modify hippocampal beta-EP content. When LY 117018 was administered together with 17 beta-estradiol in ovx animals, a clear anti-estrogenic effect in all organs and in plasma was observed, resulting in significantly lower beta-EP content with respect to the group treated with 17 beta-estradiol alone (p < 0.01). The chronic administration of LY 117018 in fertile rats significantly decreased beta-EP content in the anterior pituitary, hippocampus and plasma (p < 0.01), while it increased beta-EP hypothalamic content and did not change beta-EP content in the neurointermediate lobe. In conclusion, raloxifene analog LY 117018 has an estrogen-like action on neuroendocrine opiatergic pathways when administered alone in ovx rats, while it exerts an anti-estrogen effect in fertile or in ovx rats treated with 17 beta-estradiol.
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PMID:Raloxifene analog LY 117018 effects on central and peripheral beta-endorphin. 1053 60

The pituitary is a complex gland and is composed of several cell types, each responsible for the production of specific hormones. In the past, it was thought that one cell could make only one hormone; the concept of plurihormonality was poorly understood. Plurihormonal adenomas were thought to be either composed of multiple cell types, each producing one hormone (plurimorphous adenomas) or composed of poorly differentiated cells that exhibited abnormal production of multiple hormones. However, the molecular factors that determine hormone production have now been identified as transcription factors that target specific hormone genes. These factors have clarified three main pathways of cell differentiation. ACTH-producing corticotrophs are determined by corticotropin upstream transcription-binding element (CUTE) proteins including neuroD1/beta 2. Bihormonal gonadotrophs require expression of steroidgenic factor (SF)-1. The complex family of Pit-1 expressing cells can mature into somatotrophs, mammosomatotrophs, lactotrophs or thyrotrophs with the additional expression of estrogen receptor (ER) alpha, which enhances PRL secretion, or thyrotroph embryonic factor (TEF) which stimulates TSH-beta production. The recognition of these molecular determinants of adenohypophysial cytodifferentiation has clarified the patterns of plurihormonality which have been recognized in pituitary adenomas and provide a framework for classification of these tumors.
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PMID:Molecular determinants of pituitary cytodifferentiation. 1108 Nov 94

A single dose (3 microg) beta-endorphin was administered to newborn female and male rats (hormonal imprinting). In adult age (at 5 months) sexual behavior, steroid hormone binding capacity and brain serotonin content was studied. Females' sexual activity (lordosis quotient) significantly decreased and more animals protested against mounting (ratio of kicking and crying 21/24 vs. 8/24; p < 0.001). Males' sexual activity did not change, however more males were aggressive (4/10 vs. 1/10). Uterine estrogen receptor density significantly increased and affinity decreased. There was no change in the binding capacity of thymic glucocorticoid receptors. In the brain, five regions were studied for serotonin content. There was a gender difference in serotonin level and the intragroup differences were also high. In the endorphin treated males the serotonin level was significantly lower than in the controls. In the endorphin treated females the intragroup scattering has been significantly reduced. Nociceptin content of the cerebrospinal fluid was not changed. The experiments call attention to the possibility of adjustment of sexual and behavioral sphere by the individually different endorphin surge during labor.
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PMID:Effect of neonatal beta-endorphin imprinting on sexual behavior and brain serotonin level in adult rats. 1272 91


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