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)

An animal model using dexamethosone-suppressed, castrated dogs was developed to test the hypothesis that a pituitary hormone other than ACTH modulates adrenal androgen (AA) secretion. Plasma samples were obtained every 15 min during infusions of saline, synthetic alpha 1-24 corticotropin, porcine 1-39 corticotropin (ACTH), or bovine pituitary gland extract (PE) in a wide range of doses. Androstenedione (A), dehydroepiandrosterone (DHA), and cortisol (F) were quantified by radioimmunoassay. When the ratio of AA levels was related to those of F, in order to correct for ACTH content in the PE, the slopes of the dose-response curves for corticotropin and PE were different at the 0.01 level. For A the dose-response slope for the PE was 0.18 +/- 0.5 SE, whereas that of ACTH was 0.02 +/- 0.01. For the DHA response the slopes were 0.17 +/- 0.04 for the PE and 0.04 +/- 0.03 for ACTH. Related studies showed no increase in AA levels in response to luteinizing hormone-releasing hormone, bovine growth hormone (GH), bovine prolactin, ovine thyroid-stimulating hormone (TSH), or synthetic aqueous arginine vasopressin (AVP). We conclude that a pituitary factor other than ACTH, prolactin, GH, luteinizing hormone, follicle-stimulating hormone, TSH, or AVP may be responsible for the observed increase in AA concentrations.
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PMID:Evidence for existence of cortical androgen-stimulating hormone. 22 Aug 83

With the inrush of new data the recent clear division of neural, hormonal and immunological regulation has been seriously complicated. Both central and peripheral neural tissue produce over 30 neuropeptides, among which are many classic peptide hormones. A steroid biosynthetic pathway has been demonstrated in oligodendrocytes. However, the distribution and role of peptydoergic neurons within the reproductive system are only superficially known among farm animals. Neurons have receptors for many hormones and interleukins. Cells of the immune system, in addition to secretion of many interleukins and interferons, produce neuropeptides locally and they possess specific receptors for them as well. Till now, the interaction between the nervous, hormonal and immunological systems has not been taken into account while investigating the functions of ovarian follicles, the corpus luteum, oviduct and uterus. The penetration of blood and lymphatic vessels by hormones, neuropeptides and cytokins has not been taken into consideration also. The counter current transfer of many steroid and peptide hormones from ovarian venous and lymphatic effluent to arterial blood supplying the ovary and through arterial anastomoses of the oviduct and uterus has been hithero shown. It has been demonstrated that thanks to this system, arterial blood supplying the uterus and oviduct has, in physiological conditions, a much higher level of some steroid hormones such as progesterone and androstendione, 37% and 36% respectively, than in systemic blood. Recently, a powerful exchange system for resupplying hormones to the brain which is dependent on the phase of the estrous cycle, has been discovered. It has also been demonstrated that neuropeptides LH-RH, beta-endorphin and oxytocin as well as the steroid hormone progesterone, were counter current transferred from venous to arterial blood at the perihypophyseal cavernous sinus and carotid rete in sheep and gilts, but only during specific periods of reproductive activity. The mechanism of this process is still unknown. The role of peptydoergic neurons and cytokins in vascular permeability during hormone counter current transfer in the broad ligament vasculature, perihypophyseal cavernous sinus and carotid rete has not been investigated. It is suggested that progress in this area may change our point of view on many basic regulatory mechanisms involved in animal reproductive physiology.
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PMID:New pathways in animal reproductive physiology frontiers and perspectives. 134 74

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

Parturition in sheep is initiated by increases in activity of the fetal hypothalamic-pituitary-adrenal axis. We have previously reported that cortisol negative feedback efficacy is decreased at the end of gestation. The present study was designed to test the hypothesis that increasing plasma estrogen and/or androgen concentrations in the fetus might increase plasma adrenocorticotropic hormone (ACTH) concentration, either by stimulating ACTH secretion or by altering the negative feedback effect of cortisol on ACTH. Fetal sheep were chronically catheterized and treated with no steroid (control), 17beta-estradiol, or androstenedione (each approximately 0.24 mg/day). After catheterization and implantation of steroid pellet, fetuses were subjected to two short (10 min) periods of sodium nitroprusside-induced hypotension with or without pretreatment with intravenous infusion of hydrocortisone sodium succinate (0.5 microg/min) to test fetal ACTH responsiveness to stress and cortisol negative feedback efficacy. Estradiol treatment significantly increased basal plasma ACTH and cortisol concentrations relative to control fetuses but did not interfere with the inhibition of ACTH secretion by cortisol. Fetal plasma ACTH responses to hypotension were significantly suppressed approximately 60% in both control and estradiol-treated groups. Androstenedione treatment significantly increased basal fetal plasma ACTH and decreased basal fetal plasma cortisol concentration. Androstenedione did not alter stimulated levels of fetal ACTH but did block the inhibition of stimulated ACTH by cortisol. We conclude that increased fetal cortisol and ACTH secretion at the end of gestation may be due to the combined effects of the gonadal steroids in that estradiol increases basal plasma ACTH secretion while androstenedione reduces cortisol negative feedback efficacy.
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PMID:Modulation of ovine fetal adrenocorticotropin secretion by androstenedione and 17beta-estradiol. 914 11

Increased extraglandular aromatization has been reported as the cause of familial gynecomastia. We studied a kindred with aromatase excess inherited in an autosomal dominant manner, in which affected males had heterosexual precocity and/or gynecomastia, and affected females had isosexual precocity and/or macromastia. The propositus was a 9-yr-old boy with gynecomastia. His 7.5-yr-old sister had precocious puberty, and their father and paternal grandmother had peripubertal gynecomastia and macromastia, respectively. Serum concentrations of gonadal and adrenal steroid hormones were determined before and after the administration of corticotropin and/or hCG. Aromatase activity was determined by [3H]delta4-androstenedione to [3H]estrone conversion by cultured skin fibroblasts and/or Epstein-Barr virus-transformed lymphocytes and was detected by immunohistochemistry and/or Western analysis. Linkage was examined with a polymorphism of the aromatase (P450arom) gene. The P450arom messenger ribonucleic acid was analyzed by rapid amplification of complementary DNA (cDNA) ends, ribonuclease protection assay, and RT-PCR. hCG testing demonstrated a high rate of conversion of delta4-androstenedione to estrone and of testosterone to estradiol in the propositus and his father. Treatment of the propositus and his sister was initiated with an aromatase inhibitor (testolactone) and a GnRH analog, which successfully delayed skeletal and pubertal development in both children. Markedly increased aromatase activity was found in the patients' fibroblasts and Epstein-Barr virus-transformed lymphocytes. The P450arom polymorphism segregated with the disease in the family. A new 5'-splice variant was present in the patients' P450arom messenger ribonucleic acid, thus identifying yet another first exon of this gene, which appears to be aberrantly expressed in this family. In conclusion, a family with the aromatase excess syndrome is described, in which the condition was inherited in an autosomal dominant manner, led to feminizing manifestations in both sexes, and was associated with the aberrant utilization of a novel transcript of the P450arom gene.
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PMID:The aromatase excess syndrome is associated with feminization of both sexes and autosomal dominant transmission of aberrant P450 aromatase gene transcription. 954 66

The roles of androgen hypersecretion, in situ enzyme activity, and androgen receptors in androgenetic alopecia in women are still a matter of debate. We studied 187 women with alopecia, which we graded I, II, or III, according to Ludwig's classification, and 21 healthy control women. All participants were subjected to full basal and 1 h post-beta-1-24 corticotropin stimulation endocrine profiles. Abnormal hormone profiles were observed in 67% of the patients with alopecia alone (group A, n = 110) and in 84% of the patients with alopecia plus other symptoms of hyperandrogenism including acne, hirsutism, and menstrual cycle disturbances (group B, n = 77). Mean serum 5alpha-androstane-3alpha,17beta-diol glucuronide (3alpha-AdiolG) levels in all three patient groups (6.50+/-4.10, 8.90+/-5.80, and 14.70+/-8.90 nmol/l, respectively) correlated with the grade of alopecia (I-III) and were significantly higher than in the control group (4.80+/-2.05 nmol/l, P < 0.005). Mean serum sex hormone-binding globulin (SHBG) levels were inversely correlated with the grade of alopecia (I-III) and were significantly lower in all three patient groups (50.55+/-23.50, 40.00+/-17.65, and 38.80+/-14.10 nmol/l, respectively) than in the control group (61.15+/-17.65 nmol/l, P < 0.05). Mean serum levels of delta4-androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate, and 3alpha-AdiolG were higher in group B than in group A, and higher in group A than in the control group. The significant correlations found between adrenal secretion - either positive (with 3alpha-AdiolG levels and the body mass index) or negative (with SHBG levels) - might reflect the important contribution of secretory and metabolic components in the development of alopecia, the severity of which has been shown to be very closely related to observed levels of two of these parameters (3alpha-AdiolG and SHBG).
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PMID:Role of androgens in female-pattern androgenetic alopecia, either alone or associated with other symptoms of hyperandrogenism. 1121 20

The etiologic diagnosis of hirsutism is often difficult. Previous studies have reported normal basal androgen and SHBG concentrations in 33-50% of hirsute women, suggesting the presence of an "idiopathic" form of hirsutism as the most frequent cause of this problem. The recent use of GnRH-analogues together with the corticotropin stimulation test allows better understanding of whether the cause of hirsutism is androgen excess and, if so, whether the origin of the latter is ovarian, adrenal or both. The present study evaluated adrenal and ovarian function in 48 young hirsute women as well as in 78 normal women matched for body mass index and age, who acted as control group. To determine ovarian function, a single 100-microg dose of GnRH analogue triptorelin was injected s.c.; thereafter, gonadotropins, 17-hydroxyprogesterone (17-OHP), delta4-androstenedione (delta4), total testosterone (T) and estradiol were determined. To better understand the adrenal function, 250 microg of 1,24 ACTH were administrated as i.v. infusion for 5 h, and plasma cortisol (F), 17-OHP, A4, DHEAS, T, 11-desossicortisol were measured. The combined use of these two stimulation tests was able to detect mild to moderate abnormalities in the steroidogenesis of ovaries alone (23%), adrenals alone (16.6%), or both (35.4%) in most hirsute women (75%) with otherwise normal baseline androgen concentrations. In particular, patients showed significantly increased responses of 17-OHP, delta4, total T, 11-desossicortisol, and F to 1,24-ACTH administration. Moreover, they also had significantly higher 17-OHP and T responses to triptorelin. In conclusion, milder forms of functional ovarian and/or adrenal hyperandrogenism, similar to those found in clearly hyperandrogenic women, were observed and could be an underlying mechanism of idiopathic hirsutism.
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PMID:Functional hyperandrogenism detected by corticotropin and GnRH-analogue stimulation tests in women affected by apparently idiopathic hirsutism. 1150 82