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)

The distribution and density of selectively labeled mu-, delta-, and kappa-opioid binding sites were examined by in vitro radioautography in the hypothalamus of normal, estradiol valerate (EV)-injected, and estradiol (E2)-implanted female rats. Hypothalamic beta-endorphin concentration was also examined by RIA in these three groups of animals. Quantitative analysis of film radioautographs demonstrated a selective increase in mu-opioid binding in the medial preoptic area of EV-treated, but not of E2-implanted rats. However, both these estrogenized groups exhibited a reduction in the density of delta-opioid binding in the suprachiasmatic nucleus. Statistically significant changes between either estrogenized groups were not observed for kappa-opioid binding. Results on the hypothalamic concentration of beta-endorphin indicated a marked reduction in EV-injected animals with respect to controls. In contrast, the E2-implanted animals exhibited beta-endorphin concentrations similar to controls. The present results confirm the increase in opioid receptor binding previously reported in the hypothalamus of EV-treated rats and further demonstrate that this increase is confined to the medial preoptic area and exclusively concerns mu-opioid receptors. The concomitant reduction in beta-endorphin levels observed in the same group of animals suggests that the observed increase in mu-opioid binding could reflect a chronic up-regulation of the receptor in response to compromised beta-endorphin input. Given the restriction of this effect to the site of origin of LHRH neurons and the demonstrated inhibitory role of opioids on LHRH release, it is tempting to postulate that such up-regulation could lead to the suppression of the plasma LH pattern that characterizes polycystic ovarian disease in the EV-treated rat.
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PMID:Alterations in opioid parameters in the hypothalamus of rats with estradiol-induced polycystic ovarian disease. 217 40

Several reports have shown elevated circulating beta-endorphin (beta-EP) levels in patients with polycystic ovarian disease (PCOD). However, it is not yet clear whether these high beta-EP levels are linked to the etiopathogenesis of PCOD or are secondary to the obesity. In the present study we measured beta-EP plasma concentrations in 19 PCOD patients, 10 with normal weight (Group A) and 9 with excessive weight (Group B), and in 18 normally ovulating women, 10 with normal weight (Group C) and 9 with excessive weight (Group D). beta-EP values were similar in the two groups of non-obese patients and controls. beta-EP concentrations were also similar in the two groups of obese patients and controls, and they were significantly higher (p less than 0.05) than in non-obese patients. Our data indicate that in PCOD, elevated beta-EP values are related to obesity, suggesting that they are not linked to the pathogenesis of PCOD.
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PMID:Plasma beta-endorphin levels in obese and non-obese patients with polycystic ovarian disease. 252 98

The natural opioid ligand, beta-endorphin, and the opioid antagonist, naloxone, were administered intracerebroventricularly (i.c.v.) to evaluate effects on LH secretion in ovariectomized ewes and in ovariectomized ewes treated with oestradiol-17 beta plus progesterone either during the breeding season or the anoestrous season. Ovary-intact ewes were also studied during the follicular phase of the oestrous cycle. Jugular blood samples were taken at 10-min intervals for 8 h and either saline (20-50 microliters), 100 micrograms naloxone or 10 micrograms beta-endorphin were injected i.c.v. after 4 h. In addition, luteal phase ewes were injected i.c.v. with 25 micrograms beta-endorphin(1-27), a purported endogenous opioid antagonist. In ovariectomized ewes, irrespective of season, saline and naloxone did not affect LH secretion, but beta-endorphin decreased the plasma LH concentrations, by reducing LH pulse frequency. The effect of beta-endorphin was blocked by administering naloxone 30 min beforehand. Treating ovariectomized ewes with oestradiol-17 beta plus progesterone during the breeding season reduced plasma LH concentrations from 6-8 micrograms/l to less than 1 microgram/l. In these ewes, saline did not alter LH secretion, but naloxone increased LH pulse frequency and the plasma concentrations of LH within 15-20 min. During anoestrus, the combination of oestradiol-17 beta plus progesterone to ovariectomized ewes reduced the plasma LH concentrations from 3-5 micrograms/l to undetectable levels, and neither saline nor naloxone affected LH secretion. During the follicular phase of the oestrous cycle, naloxone enhanced LH pulse frequency, which resulted in increased plasma LH concentrations; saline had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Seasonal and steroid-dependent effects on the modulation of LH secretion in the ewe by intracerebroventricularly administered beta-endorphin or naloxone. 252 42

The basal levels of beta-endorphin were measured in 43 women with various grades of hirsutism. The degree of the hair growth, weight, body mass index (BMI), age, menstrual regularity and various androgen or pituitary hormone values were not sufficient to distinguish the patients with regard to their beta-endorphin levels. In 11 patients a clinical diagnosis of a polycystic ovarian disease-like disorder was made. The beta-endorphin values of these women did not differ from those of 10 women with adrenal hyperandrogenism or the other hirsute women with identical BMI. Plasma beta-endorphin was significantly higher in obese hirsute patients with a low testosterone/sex-hormone-binding globulin (T/SHBG) ratio than in lean, nonhirsute women with a higher T/SHBG ratio (P less than 0.02). The findings suggest a possible but complex connection of beta-endorphin with some forms of female hyperandrogenism.
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PMID:Beta-endorphin basal levels in hirsute women. 293 33

To determine the prevalence of the attenuated form of congenital adrenal hyperplasia (CAH) and hyperprolactinemia (HPPN) relative to polycystic ovarian disease (PCOD), 100 consecutive women presenting with the classic clinical features of PCOD were evaluated by basal hormonal profiles and subsequent adrenocorticotropic hormone (ACTH) stimulation tests. The study also sought biochemical markers for CAH other than ACTH stimulation. The prevalences were found to be as follows: PCOD, 65%; PCOD with HPPN, 9%; HPPN, 3%, end-organ hypersensitivity (EOH), 4%; homozygotic CAH, 4%; and heterozygotic CAH, 15%. Other than the differential response to ACTH, the only other biochemical markers observed for homozygotic CAH were significantly higher basal levels of testosterone (T) and 17 alpha-hydroxyprogesterone (17-OHP). Luteinizing hormone/follicle-stimulating hormone ratio, androstenedione, and dehydroepiandrosterone sulfate all showed no significant differences between homozygotic CAH, heterozygotic CAH, HPPN, PCOD, and EOH. This study establishes the relative prevalences of the syndromes commonly mimicking PCOD. We also conclude that the observed low incidence of CAH does not justify routine ACTH testing on all patients presenting with features of PCOD--however, our data suggest that patients with basal serum levels of T and 17-OHP greater than 50% above the upper limit of normal should undergo this dynamic test, especially if there are also certain clinical features suggestive of CAH.
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PMID:Prevalence of and markers for the attenuated form of congenital adrenal hyperplasia and hyperprolactinemia masquerading as polycystic ovarian disease. 301 93

In 9 women with polycystic ovarian disease (PCOD) and in 11 control subjects at the follicular phase of the normal cycle, blood samples were collected at 15-min intervals during a 2 h period of bed rest for the assay of beta-endorphin, beta-lipotropin, corticotropin, cortisol and prolactin. During the study period, the plasma levels of these hormones decreased more significantly in the PCOD than in the control group, suggesting that the PCOD patients had a more significant stress response to the puncture of the vein than the control subjects. The second hour of the study period was considered to represent resting levels of hormones. The mean resting levels (+/- S.E.) of the hormones between the PCOD and control groups, respectively, were as follows: beta-E, 2.0 +/- 0.4 vs. 1.1 +/- 0.1 pmol/l, p less than 0.05; beta-LPH, 3.4 +/- 0.6 vs. 2.1 +/- 0.5 pmol/l, N.S.; corticotropin, 2.0 +/- 0.3 vs. 1.1 +/- 0.5 pmol/l, p less than 0.05; cortisol, 176 +/- 24 vs. 128 +/- 16, N.S.; and prolactin; 3.9 +/- 0.6 vs. 5.6 +/- 1.2 ng/ml, N.S. These results confirm the previous findings on increased circulating levels of beta-E in PCOD. A concomitant increase of the plasma level of corticotropin suggests that the basal secretion of both beta-E and corticotropin from the anterior pituitary gland is increased in women with PCOD.
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PMID:Plasma beta-endorphin, beta-lipotropin and corticotropin in polycystic ovarian disease. 303 91

The relationship of endogenous opiates in patients with polycystic ovarian disease (PCOD) and their influence on body weight was studied. The study group consisted of 19 women with PCOD. They were amenorrheic, hirsute, and hyperandrogenic, and their average weight was 124% of the ideal body weight. They had luteinizing hormone/follicle-stimulating hormone ratios greater than or equal to 2. The control group consisted of ten women with regular ovulatory menses. Plasma beta-endorphin (beta-EP) was measured by using a very specific radioimmunoassay. beta-Lipotropin (beta-LPH) was entirely removed from the sample by preincubation of the plasma with rabbit anti-beta-LPH/Sepharose complex (Pharmacia, New Brunswick, NJ). The mean +/- standard deviation of the plasma beta-EP in the control group was 70.18 +/- 18.06 pg/ml, and the mean +/- standard deviation of beta-EP in the study group was 185.6 +/- 93.4 pg/ml, which was significantly higher than the control levels (P less than 0.001). A significant correlation was also found between plasma beta-EP level and the patient's weight in the PCOD group (r = 0.462, P = 0.025). The data from this study suggest that the elevated levels of endogenous opiates may be involved in the pathophysiology of PCOD and be related to inappropriate secretion of gonadotropins influencing body weight.
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PMID:Elevated plasma levels of beta-endorphin in a group of women with polycystic ovarian disease. 609 52

This study was carried out to document the postpubertal presentation of congenital adrenal hyperplasia (CAH), to elaborate the diagnostic criteria for it, and to investigate family members of CAH patients. Serum 17-hydroxyprogesterone (17OHP) was measured in normal women and 25 hirsute oligomenorrheic patients, five of whom were shown to have CAH. These five CAH patients, as a group, had significantly elevated levels of 17OHP when compared to normal and hirsute women, although the other 20 hirsute oligomenorrheic women also had higher levels of 17OHP than the follicular phase control subjects. A single intravenous bolus of 0.25 mg of adrenocorticotropic hormone (ACTH) caused much larger increased in 17OHP in all five CAH patients than in the control and hirsute women. The five CAH patients had decreased cortisol but normal 11-deoxycortisol responses to ACTH, thus indicating 21-hydroxylase deficiency (21HD). Clinically, they were indistinguishable from women with polycystic ovarian disease (PCO) and had basal serum levels of androgens and urinary 17-ketosteroids which were similar to those found in 47 other women presenting with the complaint of hirsutism. However, the androstenedione levels and androstenedione/cortisol ratios in response to ACTH were significantly higher in the five CAH patients than in both the normal and hirsute women. Of seven family members tested, two fathers and one mother had an intermediate 17OHP response to ACTH, thus suggesting heterozygosity. Human lymphocyte antigen (HLA) typing on family members indicated that the inheritance of the disorder may be linked to B antigens. Two siblings of one of the CAH patients had normal 17OHP responses to ACTH and also had a different HLA-B complement. These data document the existence of adult manifestation of CAH, due to 21 HD. This disorder presents with androgen excess and oligomenorrhea or amenorrhea and mimicks PCO. The diagnosis of it hinges upon the post-ACTH rise in 17OHP, whereas the levels of serum androgens and urinary 17-ketosteroids may be inconclusive.
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PMID:Adult manifestation of congenital adrenal hyperplasia due to incomplete 21-hydroxylase deficiency mimicking polycystic ovarian disease. 625 62

The relative contributions of the ovary and the adrenal gland to androgen overproduction in polycystic ovarian disease (PCOD) remain controversial. In this investigation, patients with proven PCOD were divided into two groups, (1) those with low dehydroepiandrosterone sulfate (DHEAS) levels and (2) those with high DHEAS levels, and compared with controls for their response to adrenocorticotropin hormone (ACTH) stimulation. Significant differences in weight, degree of menstrual disturbance, and basal progesterone levels distinguished the two groups with PCOD. Although no discrete enzyme block was unmasked by ACTH, marked differences in steroid production ratios were apparent between the low and high DHEAS PCOD groups. These results suggest that in PCOD with high DHEAS (1) substantial differences in adrenal steroidogenesis pathways occur, (2) increased progesterone as well as inappropriate estrogen feedback may contribute to chronic anovulation, and (3) serum DHEAS levels may be a helpful screen in discerning those patients who have a significant adrenal component to their hyperandrogenism and may benefit from adrenal suppression alone or in combination.
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PMID:Differential response to adrenocorticotropin hormone stimulation in polycystic ovarian disease with high and low dehydroepiandrosterone sulfate levels. 628 Oct 86

Thirty-three women with hirsutism and oligomenorrhea were stimulated with synthetic adrenocorticotropin, as well as 12 controls. Of these test subjects 20 demonstrated significantly greater rises of serum levels of 3,17-dihydroxy-5-pregnen-20-one as well as dehydroepiandrosterone sulfate suggesting an attenuated deficiency of 3 beta-hydroxysteroid dehydrogenase. Five did not show similar rises of these compounds but revealed significant elevations of 17-hydroxyprogesterone as would be expected in 21-hydroxylase deficiency. None of the subjects were virilized. Eight additional hirsute women were not different than the normals. It appears that a subtle deficiency of 3 beta-hydroxysteroid dehydrogenase may be more common as an explanation of a syndrome resembling polycystic ovarian disease than has been previously recognized.
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PMID:The response of several adrenocortical steroids to the administration of ACTH in hirsute women. 630 46


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