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)

Adrenal responsiveness was evaluated by injecting 10 multiparous dairy cows with 200 IU adrenocorticotropin between -13 and -2 days prepartum (I) and postpartum between 24 and 40 h (II) and 21 and 24 days (III). Concentrations of glucocorticoids following injection were influenced by day of injection, temperature, and minimum percent relative humidity but not by breed, breed X injection day interaction, or age of cow. Likewise differences in regressions for adrenal response and mean response (ng/ml) for the three injections were nil. Mean concentrations at peak (45, 60, and 120 min postinjection samples) adjusted for preinjection concentrations also did not differ for the three periods of injection. Mean concentrations of glucocorticoids in plasma for daily samples between -13 and -2 days prepartum were 5.3 +/- .4 (n = 61), reached a peak of 14.8 +/- .3 ng/ml the day of calving, and remained high for 2 days postpartum. Estradiol increased through prepartum sampling from 23.3 to 339.6 +/- 94.1 pg/ml the day of calving, then declined abruptly. Progestins began to decline about -5 days prepartum from mean concentration of 4.09 +/- .62 (n = 25) and attained low concentrations (.30 +/- .06 ng/ml) 2 days postpartum. Although there was a surge of glucocorticoids at parturition, this was not associated with a modification in adrenal responsiveness or with prepartum concentrations of other steroid hormones of plasma. Adrenal potential in prepartum and postpartum dairy cows appears well maintained.
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PMID:Adrenal responsiveness in pre- and postpartum dairy cows. 21 98

The effects of oral contraceptive treatment on the pituitary-adrenal axis were studied. Secretion rate and plasma concentration of the adrenocortical steroid cortisol was modified in subjects treated with estrogenic and/or progestational steroids. Concentrations of adrenocorticotropin (ACTH) and cortisol in plasma obtained at 0800-0900 hours from a group of women with normal cyclic menses (n=4) ranged from 78-120 pg/ml and 77-137 pg/ml, respectively. Although significant cyclic changes in plasma levels of luteinizing hormone (LH) follicle stimulating hormone (FSH), estradiol, and progesterone occurred during the ovarian cycle, no obvious cyclic fluctuations in plasma levels of ACTH or cortisol were observed. Plasma concentrations of women treated with Norinyl 1 + 80 (1 mg of norethindrone and .08 mg of mestranol) of LH, FSH, estradiol, and progesterone were significantly lower (P .001) than plasma levels of these hormones in normal women during the ovarian cycle. Mean daily plasma concentrations of ACTH were significantly lower ( P .001), whereas plasma cortisol levels were significantly higher (P .001) in women treated with oral contraceptives compared to the levels of these hormones in untreated ovulatory women.
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PMID:Plasma levels of adrenocorticotropin and cortisol in women receiving oral contraceptive steroid treatment. 22 73

The acute effect of weightlifting on beta-endorphin and estradiol was studied in experienced female recreational weightlifters. Five eumenorrheic females completed two months of testing, each with a different sequence of testing conditions (SEQ1 and SEQ2). In SEQ1, a week of weight maintenance diet and prescribed exercise (3 d.wk-1, 3 sets, approximately 85% 1 RM, 10-12 reps, eight lifts) beginning on d 11 of their menstrual cycle was followed by measurement of hormone response to a weightlifting bout during energy balance (EBAL) on d 18. This included blood sampling via a catheter before, just after, and at 15 and 30 min of recovery. The women consumed 500 kcal per day for the next 48 hrs and then repeated the weightlifting test during negative energy balance (NEBAL). SEQ2 was similar except that the 48 hrs of NEBAL preceded the EBAL test condition. Estradiol and beta-endorphin increased from baseline to immediately post exercise under both dietary conditions but was significant only during NEBAL. Estradiol increased 1.6 fold and beta-endorphin 3.7 fold by the end of the resistance exercise bout during NEBAL. Both hormones were also elevated for a longer time during recovery in the NEBAL condition. Since estradiol and beta-endorphin can suppress gonadotropin release, it is possible that repeated elevations in these hormones during weightlifting, especially concurrent with energy restriction, could contribute to disruption of the menstrual cycle.
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PMID:Response of beta-endorphin and estradiol to resistance exercise in females during energy balance and energy restriction. 145 50

Immunoreactive beta-endorphin (IR-beta END) is present in human endometrium. Several indirect lines of evidence suggest that endometrial beta END is under steroid hormone control, i.e. IR-beta END is detectable in the secretory, but not the proliferative, endometrium, and progesterone administration increases the concentration of IR-beta END in uterine secretions of ovariectomized gilts. To study the effect of steroid hormones on endometrial beta END, we first questioned whether Ishikawa human endometrial adenocarcinoma cells (which respond to steroid hormones) express the proopiomelanocortin (POMC) gene. Indeed, on Northern blot analysis, a RNA similar or identical in size to pituitary POMC mRNA was present in Ishikawa cell RNA extracts. IR-beta END was also present in Ishikawa cell extracts and culture medium, which coeluted with synthetic human beta END in a Sephadex G-50 column. Ishikawa cells released most of their IR-beta END into the culture medium. Estradiol decreased the release of IR-beta END from Ishikawa cells, an effect that was dependent upon dose and time. The maximal effect was observed after a 4-day exposure to 10 nM estradiol (44 +/- 6% of the control value; n = 6; P less than 0.001). This effect was almost completely counteracted by a 100-fold excess of the antiestrogen 4-hydroxytamoxifen. Progesterone and dihydrotestosterone did not have a statistically significant effect on IR-beta END release. Dexamethasone had effects similar to those of estradiol, i.e. decreased the release of IR-beta END in a time- and dose-dependent manner. The maximal effect was detected after a 4-day exposure to 10 nM dexamethasone (53 +/- 6% of the control value; n = 6; P less than 0.001). Interestingly, the antiprogestin-antiglucocorticoid RU486 exhibited agonistic properties, i.e. diminished the release of IR-beta END in a time- and dose-dependent fashion, possibly via the glucocorticoid receptor. Its maximal effect was reached after a 4-day exposure to 10 nM RU486 (55 +/- 6% of the control value; n = 6; P less than 0.001). In conclusion, our data demonstrate that the release of IR-beta END from Ishikawa cells in culture is inhibited by estradiol and dexamethasone, suggesting that endometrial beta END is under estrogen and glucocorticoid regulation, as is the case with hypothalamic and pituitary POMC-derived peptides. This is the first time that the in vitro release of a peripheral-extracranial POMC-derived peptide has been found to be under the direct control of estrogens and glucocorticoids.
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PMID:Steroid hormones regulate the release of immunoreactive beta-endorphin from the Ishikawa human endometrial cell line. 163 59

Steroid levels and ovarian follicular morphology were examined in sows on days 19 and 26 (day 5 of next cycle) after injection of adrenocorticotropic hormone (ACTH) or dexamethasone (DXM). Five sows received DXM (30 micrograms/kg bodyweight, intramuscularly) at 12 h intervals from days 9 to 14. Another five sows were given ACTH (2 IU/kg bodyweight, intramuscularly) from day 17 to day 19 or the end of estrus. Five control sows received no treatment. Ovulation occurred only in control sows and progesterone was significantly elevated at day 26. Estradiol values in ovarian vein blood were low but variable on day 19 in DXM- and ACTH-treated animals. Androstenedione values were lower (p less than 0.05) on both days in sows receiving DXM but not in those given ACTH compared to control values on day 19. Morphometric analysis, based on six follicles in each of three sows from each treatment group, indicated that follicular and antral diameters and granulosa cell numbers did not differ for either hormone treatment group on either day compared to those of control sows on day 19. The mitotic index suggested that cell replication continued. However, pyknotic and karyorrhectic nuclei were also seen in the hormone treatment groups. Follicles and oocytes from both DXM- and ACTH-treated sows showed signs of early degenerative changes including disorganization of cumulus cells and large lipid droplets in the cytoplasm of oocytes. Significant differences from control follicles in granulosa cell density and theca interna cell density suggested an association with the altered steroid hormone secretion.
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PMID:Morphometric and steroid hormone changes associated with experimental anovulatory follicles in the sow. 165 38

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

This study was designed to explore the hormonal regulation of CNS opioid peptide levels in female Sprague Dawley rats. Forty-eight animals were divided into 2 equal groups for acute and chronic studies. Each group was further divided into 4 subgroups, each containing 6 animals. Each rat in the control group received an inert pill (in 0.25 ml corn oil daily by gavage); the second group, 15 micrograms norethindrone (NE, a potent progestin present in the oral contraceptive Micronor); the third group, 15 micrograms NE and 1 microgram ethinyl estradiol, EE2 (present in the oral contraceptive Modicon) and the fourth group, 10 times the dose of the third group. Rats were treated either acutely for 5 days or chronically for 7 weeks. Opioid peptides were estimated by radioimmunoassay. Acute administration of 150 micrograms NE + 10 micrograms EE2 decreased the levels of methionine-enkephalin (ME), leucine-enkephalin (LE), dynorphin (DYN) and beta-endorphin like immunoreactivity (beta-EI) by about 50% in the pituitary. The same dose on chronic administration also decreased DYN, but increased the levels of ME and LE in the pituitary by 331 and 69%, respectively. In the hypothalamus, chronic administration of NE + EE2 increased the level of ME (155%) and LE (87%) as well as of DYN (97%). In the striatum, the levels of LE (33%) and DYN (115%) were elevated during chronic administration. It is concluded that the acute administration of NE + EE2, in general, reduces the levels of ME, LE, DYN and beta-EI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of oral contraceptives on the rat brain and pituitary opioid peptides. 286 95

The effect of chronic administration of adrenocorticotropin on ovarian follicular development was studied. Twelve nonlactating Holstein cows received either 100 IU adrenocorticotropin (n = 6) or saline (n = 6) at 12-h intervals, commencing d 16 and continuing until d 23 of an induced estrous cycle (estrus = d 0). Cows were slaughtered on d 24, ovaries collected, and number of visible antral follicles recorded. Estradiol-17 beta, androstenedione, and testosterone in follicular fluid, and luteinizing hormone and follicle-stimulating hormone receptors in follicular tissue of the largest follicles were determined. Largest follicles were classified as ovulatory or nonovulatory based on the estrogen to androgen ratio. One cow treated with adrenocorticotropin, but none treated with saline, had ovulated by slaughter. The numbers of small, medium, and large antral follicles were 0, 1, and 5 for cows treated with adrenocorticotropin and 0, 1, and 6 for cows treated with saline. Follicular diameter (15.0 +/- 1.0 versus 14.0 +/- 2.0 mm) and follicular fluid volume (2.9 +/- .8 versus 2.2 +/- .5 ml) of the largest follicle in cows treated with adrenocorticotropin or saline were not different. No differences were found in the number of luteinizing hormone and follicle stimulating hormone receptors nor in the proportion of ovulatory versus nonovulatory follicles between treatments. We conclude that adrenocorticotropin administered at 100 IU every 12 h during the follicular phase does not significantly alter follicular development in the nonlactating dairy cow.
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PMID:Follicular development after administration of adrenocorticotropin to nonlactating Holstein cows. 301 65

The authors present a case report that provides support for a relationship between estrogen and the menstrual cycle on the 1 hand and affective disorders on the other. The patient in this case, a 35-year old woman, suffered from a rapid cycling affective disorder that was severely affected by her menstrual cycle and responded positively to oral contraceptives (OCs). The patient had a 24-year history of numerous manic and depressive episodes, the 1st of which coincided with menarche. She had noted that, 4 days before menses, she would experience symptoms of premenstrual tension syndrome (PMS) and often the onset of an affective episode. Treatment with a series of psychotropic agents had not been effective in controlling the number of episodes. However, the patient reported that there had been an 8-9-month period in the past when she had taken OCs and had fewer symptoms. Thus, the patient was placed on Ortho-Novum as well as imipramine. At the 9-month follow-up, she reported there had been no further episodes of depression or mania. The exact mechanism behind estrogen's psychotropic effect is unclear, although it increases the central availability of norepinephrine and induces changes in dopaminergic, noradrenergic, and serotonergic receptors. Beta-endorphin levels covary with estrogen levels, and estrogen seems to affect every major neurotransmitter system. The fact that estrogen has not consistently been shown to be effective in this regard may only signify the existence of a distinct subclass of affective disorders closely linked to the menstrual cycle. This subclass may have some type of dysfunction within the hypothalamic-pituitary-gonadal axis that contributes to mood swings.
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PMID:Antidepressant effects of estrogen. 405 18

Fifteen women with idiopathic hirsutism (N = 11) or hirsutism with androgen excess (N = 4) were treated by Cyproterone acetate orally (50 mg from the 5 th to the 25 th day of the menstrual cycle) and Ethinyl Estradiol (day 15-25). Hirsutism was improved in 86% of cases with progressive improvement at 3, 6, 12 months. At 12 months, the clinical score for hirsutism was 56% of the original score. Disturbance of menstrual cycles was more frequent than reported with Hammerstein's pattern of treatment. Clinical and biological tolerance was good. delta 4 androstenedione decreased significantly at 6 months (respectively 2,26 ng/ml - 1,25 ng/ml). There was no significant decrease of plasma testosterone. Result of B 1-24 corticotropin test remained normal after 12 months of treatment.
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PMID:[Cyproterone acetate. 15 cases of hirsutism treated for 1 year]. 623 50


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