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)

A single dose of 0.5 micrograms beta-endorphin injected intraventricularly in unanesthetized male rats bearing chronic intraventricular and intrajugular cannulas led to a sevenfold stimulation of plasma prolactin (PRL) levels 10 to 20 min after injection of the peptide, while a dose of 2 micrograms of beta-endorphin led to a comparable stimulation of plasma growth hormone (GH) concentration. Met-Enkephalin was much less potent than beta-endorphin in stimulating PRL and GH release. Naloxone, a specific opiate antagonist, completely blocked the stimulation of GH and PRL release at the doses of 0.5 and 12.5 mg/kg, respectively. beta-Endorphin and Met-enkephalin from 41 discrete brain nuclei were measured by radioimmunoassay (RIA). beta-Endorphin was found in the hypothalamus medial preoptic nucleus, nucleus interstitialis striae terminalis (NIST), nucleus medialis thalami, and periaqueductal gray. Met-Enkephalin was found predominantly in the globus pallidus, NIST, medial preoptic nucleus, nucleus amygdaloideus centralis, and nucleus lateralis hypothalami. Treatment with both estrogens and haloperidol led to differential effects on Met-enkephalin content in various brain nuclei. Estrogen treatment increased Met-enkephalin levels in globus pallidus, NIST, medial and lateral preoptic nuclei, and periaqueductal gray, while a decrease of the Met-enkephalin content in the nucleus amygdaloideus centralis was found. Haloperidol treatment led to a stimulatory effect in striatum, medial and lateral preoptic nuclei, and interpeduncular nucleus.
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PMID:beta-Endorphin and met-enkephalins: their distribution, modulation by estrogens and haloperidol, and role in neuroendocrine control. 738 27

The opioids beta-endorphin and the dynorphins belong to two separate families of endogenous opioid peptides (EOP). They are produced not only in the central nervous system but also in nonneural tissues where, as it appears, they act locally via paracrine mechanisms. These opioids have been shown to be produced at multiple sites along the mammalian reproductive tract including the intrauterine cavity. The aim of the present work was to find out if the well differentiated human endometrial cell line of Ishikawa, which has been shown to be a good in vitro model for the study of the effects of steroid hormones on human epithelial endometrium, expresses these two EOP. Northern blot hybridization of RNA from these cells showed the presence of a 1.2-kb POMC and a 2.4-kb PDYN transcript. Radioimmunoassay and gel filtration chromatography characterization of the immunoreactive (IR) opioid peptides present in the culture media showed the presence of IR-beta-endorphin and IR-dynorphins. The apparent molecular weight of IR-beta-endorphin was that of authentic beta-endorphin while the bulk of the IR-dynorphin had an apparent molecular weight of 8 kd. The secretion of both opioids could be increased by KCl-induced depolarization. Estrogen and glucocorticoids decreased, in a dose- and time-dependent manner, the secretion of beta-endorphin from the Ishikawa cells while progesterone and dihydrotestosterone did not have a statistically significant effect. The antiprogestin-antiglucocorticoid RU486 acted as an agonist, i.e., it diminished beta-endorphin secretion possibly via glucocorticoid receptors. On the other hand, the secretion of dynorphins was not affected by any of the steroids tested while LHRH, the inducer of gonadotropins and anterior pituitary dynorphins secretion, provoked a time- and dose-dependent increase of their secretion without affecting that of beta-endorphin. These data suggest that the regulation of endometrial opioids production is type-specific. Thus, it is possible that each type of endometrial opioid participates in different local homeostatic loops and exerts distinct paracrine effects.
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PMID:Interaction between steroid hormones and endometrial opioids. 797 24

To examine mechanisms responsible for sex differences in hypothalamo-pituitary-adrenal (HPA) axis responsiveness to stress, we studied the role of androgens in the regulation of the adrenocorticotropin (ACTH) and corticosterone (CORT) responses to foot shock and novelty stressors in gonadectomized (GDX) or intact male F344 rats. Foot shock or exposure to a novel open field increased plasma ACTH and CORT, which was significantly greater in GDX vs. intacts. Testosterone (T) or dihydrotestosterone propionate (DHT) treatment of GDX animals returned poststress levels of ACTH and CORT to intact levels. Estrogen treatment of GDX males further increased poststress CORT secretion above GDX levels. There was no difference in the ACTH response of anterior pituitaries from intact, GDX, and GDX+DHT animals to CRF using an in vitro perifusion system. There were no differences in beta max or binding affinity of type I or II CORT receptors in the hypothalamus or hippocampus of intact, GDX, or GDX+DHT groups. These data demonstrate an effect of GDX on hormonal indices of stress. The increased response in GDX rats appears to be due to the release from androgen receptor mediated inhibition of the HPA axis. This inhibition by androgen is not due to changes in anterior pituitary sensitivity to CRH, nor to changes in type I or type II corticosteroid receptor concentrations.
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PMID:Androgen regulation of adrenocorticotropin and corticosterone secretion in the male rat following novelty and foot shock stressors. 814 Jan 54

Estrogen and progesterone are the most important ovarian steroid hormones regulating female fertility. They have a profound effect on the central nervous system. Target functions of sex steroids in the brain are: pituitary and hypothalamic hormone release, thermoregulatory and cardiocirculatory activities and behavior and mood changes. Furthermore, several studies have shown a correlation between brain neurotransmitters, neuropeptides and sex steroid hormones: they influence synthesis and release of norepinephrine, dopamine, serotonin, gonadotropin releasing hormone, beta-endorphin, corticotropin releasing factor and prolactin. Thus, oral hormone contraceptives inhibit the ovulatory process by blocking the activity of the hypothalamus-pituitary-gonadal axis. This inhibitory effect seems to be due to the action of both estrogens and progestins.
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PMID:Effects of sex steroid hormones on the neuroendocrine system. 967 10

The aim of the study was to compare the immunoreactivity of estrogen receptors (ER) and chromogranin-A (CHR-A) in human prolactinomas with verified plurihormonality. Eleven cases of prolactinomas, nine found in women aged from 15-32 and two found in two men both aged 54 years, were analyzed for possible colocalization of other hormones produced by adenohypophysis, i.e. growth hormone (GH), thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH) and adrenocorticotropic hormone (ACTH). All evaluated cases of prolactinomas were clinically manifested by elevated values of prolactin (PRL) in patient serum, while the values of other assayed hormones were within the normal range. Although biopsy material is not routinely submitted to immunohistochemical analysis for plurihormonality, these eleven cases of operated prolactinomas were randomly examined to the presence of plurihormonality. In six cases of prolactin-producing adenomas, the coexistence of growth hormone was detected. Colocalization of follicle-stimulating hormone and weak expression of adrenocorticotropic hormone were found in two cases each. Thus, bihormonal activity (PRL + GH) was found in six, and trihormonal activity (PRL + GH + FSH and PRL/GH + ACTH) in three cases of prolactinoma. In addition, the presence of prolactin and growth hormone was demonstrated in morphologically different cells. Eight of these eleven pituitary adenomas were tested for estrogen receptors (ER), which play an important role as growth stimulating factors and secretory factors for prolactin-producing cells. We tried to determine if there was a difference in the intensity of expression of estrogen receptors and chromogranin-A between pure prolactinomas and mixed, plurihormonal prolactinomas. By use of monoclonal antibodies, chromogranin-A found to be reactive in seven of eleven prolactinomas, i.e. in plurihormonal prolactinomas. Estrogen receptors were markedly expressed in all the eight prolactinomas analyzed, which may prove significant in the treatment of these hypophyseal tumors.
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PMID:Comparative immunohistochemical analysis of estrogen receptor and chromogranin-A reactivity in plurihormonal human prolactinomas. 1102 10

Estrogen regulates hypothalamic gene expression, synthesis and release of the endogenous opioid peptide beta-endorphin (betaEND), although a consensus estrogen response element sequence has not been identified in the rat proopiomelanocortin (POMC) gene. POMC gene expression is also regulated by the activation of AP-1 promoter elements, which are known to be estrogen sensitive. The present studies examine whether estrogen modulates the hypothalamic POMC system through a non-classical mechanism involving AP-1 binding proteins such as cFos. Immunohistochemical double-labeling for betaEND and cFos was used and immunoreactive (-ir) populations were quantified in the arcuate nucleus and periarcuate area across time using unbiased stereological methods. Ovariectomized rats were injected with 50 microg estradiol (E2), 500 microg tamoxifen citrate (TAM) or both (E2+TAM) and were perfused 1, 2, 4 or 48 h later. E2 rapidly increased numbers of cFos-ir, betaEND-ir and doubly-labeled cells after 4 h, and the number of betaEND-ir cells remained high 48 h later, suggesting that the stimulatory effects of cFos on POMC in the hypothalamus persist after the cFos signal decays. Treatment with TAM alone did not affect the numbers of immunoreactive cells, although E2+TAM blocked the E2-mediated induction in all immunoreactive populations. Similar effects were seen at the transcriptional level. E2 increased hypothalamic POMC mRNA after 4 h, while TAM treatment or coadministration of E2+TAM did not significantly change the levels of POMC mRNA. Cellular colocalization of betaEND-ir and cFos-ir supports a possible intracellular co-regulation of these peptides by an estrogen-dependent mechanism within a subset of hypothalamic neurons. It does not, however, appear that E2 acts directly through an AP-1 site within the POMC gene.
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PMID:Estrogen and tamoxifen differentially regulate beta-endorphin and cFos expression and neuronal colocalization in the arcuate nucleus of the rat. 1112 86

The mu-opioid receptor (MOR), a G-protein-coupled receptor, is internalized after endogenous agonist binding. Although receptor activation and internalization are separate events, internalization is a good assay for activation because endogenous opioid peptides all induce internalization. Estrogen treatment of ovariectomized rats induces MOR internalization, providing a neurochemical signature of estrogen activation of the medial preoptic nucleus. MOR activation appears to be the mechanism via which estrogen acts in the medial preoptic area to prevent the display of female reproductive behavior during the first 20-24 hr after estrogen treatment. Naltrexone, an alkaloid universal opioid receptor antagonist, prevented MOR internalization, suggesting that estrogen induces the release of endogenous opioid peptides that in turn activate the MOR. Enkephalins and beta-endorphin are nonselective endogenous MOR ligands. The most selective endogenous MOR ligands are the endomorphins. Infusions of selective MOR agonists, H-Tyr-d-Ala-Gly-N-Met-Phe-glycinol-enkephalin (DAMGO) or endomorphin-1, into the medial preoptic nucleus attenuated lordosis, and their effects were blocked with the MOR antagonist H-d-Phe-Cys-Tyr-d-Trp-Orn-Thr-Pen-Thr-NH(2) (CTOP). Infusion of endomorphin-1 internalized MOR. To determine whether progestin also acts via the MOR system to facilitate reproductive behavior, ovariectomized rats were primed with 17beta-estradiol and progesterone. Progestin facilitation of lordosis was correlated with a reduction of estrogen-induced MOR internalization. Progestin reversed estrogen-induced MOR internalization, suggesting that progesterone blocked estrogen-induced endogenous opioid release, relieving estrogen inhibition and facilitating lordosis. These results indicate a central role of MOR in the mediation of sex steroid activation of the CNS to regulate female reproductive behavior.
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PMID:Progesterone blockade of estrogen activation of mu-opioid receptors regulates reproductive behavior. 1146 44

To assess the effect of transdermal estrogen substitution on the hypothalamic-pituitary-adrenal (HPA) axis responsiveness/sensitivity and the impact of the antrophometric characteristics on these parameters, 20 postmenopausal women seeking treatment for the relief of postemenopausal symptoms were studied. They received transdermal 50 microg/d estradiol for 12 weeks (estrogen replacement therapy [ERT]). Patients were classified as low waist-to-hip ratio (WHR) (peripheral fat distribution women; n = 12) and high WHR (central fat distribution women; n = 8) according to the cut-off value of 0.85. Plasma hormone and lipid concentration were assessed at baseline and after 12 weeks of treatment. Results were compared with a group of 8 placebo-treated patients who served as controls. Corticotropin (ACTH) and cortisol (F) were expressed as fasting values, area under the curve (AUC), and time course over 90 minutes after corticotropin-releasing hormone (CRH) intravenous (IV) bolus (1 microg/kg body weight [BW]). Adrenal sensitivity to CRH stimulus was expressed as time course over 90 minutes and AUC of the F/ACTH molar ratio. The plasma F levels in response to ACTH stimulation did not change after ERT; however, a highly significant improvement of adrenal sensitivity was observed (P <.01). In fact, estrogen treatment significantly decreased the amount of ACTH produced after CRH stimulation, both as absolute time course and AUC (P <.01). No significant change was observed in controls. Considering body fat distribution, the high WHR group showed higher ACTH (P <.01), lower F/ACTH values, and superimposable F plasma values compared with the low WHR group. Estrogen treatment induced a significant ACTH reduction after CRH (P <.01) only in the high WHR group, whereas cortisol response was similar in both groups both before and after treatment. A significant negative correlation was found between WHR and adrenal sensitivity before treatment. ERT significantly improved adrenal sensitivity only in the low WHR group (P <.01). These data suggest that different mechanisms can prevail in the control of the HPA axis in menopause. Estrogens could exert different effects on the hypothalamic-pituitary axis, as well as on adrenal function, and these changes seem to be partially dependent on the pattern of body fat distribution.
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PMID:Estrogen treatment and body fat distribution are involved in corticotropin and cortisol response to corticotropin-releasing hormone in postmenopausal women. 1183 38

Here we report on the progress we have made in elucidating the mechanisms through which estrogen alters synaptic responses in hypothalamic neurons. We examined the modulation by estrogen of the coupling of various receptor systems to inwardly rectifying and small conductance, Ca(2+)-activated K(+) (SK) channels. We used intracellular sharp-electrode and whole-cell recordings in hypothalamic slices from ovariectomized female guinea pigs. Estrogen rapidly uncouples mu-opioid receptors from G protein-gated inwardly rectifying K(+) (GIRK) channels in beta-endorphin neurons, manifest by a reduction in the potency of mu-opioid receptor agonists to hyperpolarize these cells. This effect is blocked by inhibitors of protein kinase A and protein kinase C. Estrogen also uncouples gamma-aminobutyric acid (GABA)(B) receptors from the same population of GIRK channels coupled to mu-opioid receptors. At 24 h after steroid administration, the GABA(B)/GIRK channel uncoupling observed in GABAergic neurons of the preoptic area (POA) is associated with reduced agonist efficacy. Conversely, estrogen enhances the efficacy of alpha(1)-adrenergic receptor agonists to inhibit apamin-sensitive SK currents in these POA GABAergic neurons, and does so in both a rapid and sustained fashion. Finally, we observed a direct, steroid-induced hyperpolarization of both arcuate and POA neurons, among which gonadotropin-releasing hormone (GnRH) neurons are particularly sensitive. These findings indicate a richly complex yet coordinated steroid modulation of K(+) channel activity that serves to control the excitability of hypothalamic neurons involved in regulating the reproductive axis.
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PMID:Estrogen modulation of K(+) channel activity in hypothalamic neurons involved in the control of the reproductive axis. 1196 Jun 20

This study examined the in vivo relationship between expression of the HDL receptor scavenger receptor class B (SR-BI) and corresponding structural changes in the rat adrenocortical cell microvillar compartment. Using hormonal stimulation and withdrawal protocols, we were able to manipulate adrenal SR-BI levels and carry out qualitative and quantitative measurements correlating SR-BI expression with microvillar mass and microvillar channel formation. Young male rats were used as controls or treated with adrenocorticotropin hormone (ACTH) (24 h), 17alpha-ethinyl estradiol (17alpha-E2) (5 days), or dexamethasone (DEX) (24 h). Quantitative Western blot analysis and immunocytochemistry indicated that ACTH and 17alpha-E2 treatment greatly increased SR-BI expression in the adrenal (especially in the microvillar compartment of adrenocortical cells), whereas DEX treatment led to a decrease of SR-BI by all measurements. At the same time, striking ultrastructural changes occurred in the adrenocortical cell microvillar compartment: e.g., microvillar area and microvillar channel formation and complexity dramatically increased (compared with control values) after ACTH or 17alpha-E2 treatment, whereas the same values declined after DEX treatment. These measurements illustrate the exceptional flexibility and responsiveness of the microvillar compartment to hormonal stimuli, and suggest that regulation of SR-BI expression and structural configuration of the surface of steroidogenic cells goes hand in hand.
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PMID:Hormonal regulation of adrenal microvillar channel formation. 1203 60


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