beta-endorphin and Polycystic-Ovary-Syndrome

The polycystic ovary syndrome (PCOS) is a condition characterized by hyperandrogenism and chronic oligo-anovulation. However, many features of the metabolic syndrome are inconsistently present in the majority of women with PCOS. Approximately 50% of PCOS women are overweight or obese and most of them have the abdominal phenotype. Obesity may play a pathogenetic role in the development of the syndrome in susceptible individuals. In fact, insulin possesses true gonadotrophic function and an increased insulin availability at the level of ovarian tissue may favour excess androgen synthesis. Obesity, particularly the abdominal phenotype, may be partly responsible for insulin resistance and associated hyperinsulinemia in women with PCOS. Therefore, obesity-related hyperinsulinemia may play a key role in favouring hyperandrogenism in these women. Other factors such as increased estrogen production rate, increased activity of the opioid system and of the hypothalamic-pituitary-adrenal axis, decreased sex hormone binding globulin synthesis and, possibly, high dietary lipid intake, may be additional mechanisms by which obesity favours the development of hyperandrogenism in PCOS. Irrespective of the pathogenetic mechanism involved, obese PCOS women have more severe hyperandrogenism and related clinical features (such as hirsutism, menstrual abnormalities and anovulation) than normal-weight PCOS women. This picture tends to be more pronounced in obese PCOS women with the abdominal phenotype. Body weight loss is associated with beneficial effects on hormones, metabolism and clinical features. A further clinical and endocrinological improvement can also be achieved by adding insulin-sensitizing agents and/or antiandrogens to weight reduction programmes. These obviously emphasize the role of obesity in the pathophysiology of PCOS.

Topics: Androgens; beta-Endorphin; Body Composition; Diet; Estrogens; Female; Human Growth Hormone; Humans; Insulin; Luteinizing Hormone; Obesity; Polycystic Ovary Syndrome; Sex Hormone-Binding Globulin; Somatomedins

Topics: Anovulation; beta-Endorphin; Female; Gonadotropins, Pituitary; Humans; Menstruation Disturbances; Pituitary Hormone-Releasing Hormones; Polycystic Ovary Syndrome; Reproduction

The aim of study was to evaluate clinical outcome and hormone profiles of laparoscopic electroincision of the ovaries in women with polycystic ovary syndrome (PCOS) before and after treatment. Forty five clomiphene-citrate resistant women with polycystic ovary syndrome underwent laparoscopic electroincision of the ovaries. Serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), testosterone (T), androstenedione, 17 OH progesterone and beta endorphins were recorded before and 24 hours after the treatment. Clinical and reproductive outcome and hormone profiles were analyzed. Patients were observed during 12 months period. Laparoscopic electroincision of the ovaries was successfully performed without complications in all patients. LH/FSH ratio was 1,66 24 hours after treatment. Serum levels of T, androstenedione, 17 OH progesterone, and beta endorphins were significantly reduced 24 hours after laparoscopic electroincision of the ovaries. In follow-up period 87% of patients were recorded to have regular menstrual cycles and 61% pregnancy rate was achieved spontaneously. Laparoscopic electroincision of the ovaries is an effective treatment in clomiphene-citrate resistant women with polycystic ovary syndrome. The high pregnancy rate of the procedure offers a promising management for patients with polycystic ovary syndrome.

Topics: Adult; Androstenedione; beta-Endorphin; Clomiphene; Drug Resistance; Electrosurgery; Female; Fertility Agents, Female; Follicle Stimulating Hormone; Humans; Laparoscopy; Luteinizing Hormone; Menstrual Cycle; Polycystic Ovary Syndrome; Pregnancy; Pregnancy Rate; Progesterone; Testosterone; Treatment Outcome

The present study was designed to evaluate if electro-acupuncture (EA) could affect oligo-/anovulation and related endocrine and neuroendocrine parameters in women with polycystic ovary syndrome (PCOS).. Twenty-four women (between the ages of 24 and 40 years) with PCOS and oligo-/amenorrhea were included in this non-randomized, longitudinal, prospective study. The study period was defined as the period extending from 3 months before the first EA treatment, to 3 months after the last EA treatment (10-14 treatments), in total 8-9 months. The menstrual and ovulation patterns were confirmed by recording of vaginal bleedings and by daily registrations of the basal body temperature (BBT). Blood samples were collected within a week before the first EA, within a week after the last EA and 3 months after EA.. Nine women (38%) experienced a good effect. They displayed a mean of 0.66 ovulations/woman and month in the period during and after the EA period compared to a mean of 0.15 before the EA period (p=0.004). Before EA, women with a good effect had a significantly lower body-mass index (BMI) (p<0.001), waist-to-hip circumference ratio (WHR) (p=0.0058), serum testosterone concentration (p=0.0098), serum testosterone/sex hormone binding globulin (SHBG) ratio (p=0.011) and serum basal insulin concentration (p=0.0054), and a significantly higher concentration of serum SHBG (p=0.040) than did those women with no effect.. Repeated EA treatments induce regular ovulations in more than one third of the women with PCOS. The group of women with good effect had a less androgenic hormonal profile before treatment and a less pronounced metabolic disturbance compared with the group with no effect. For this selected group EA offers an alternative to pharmacological ovulation induction.

Topics: Adult; Androgens; Anovulation; beta-Endorphin; Body Constitution; Body Mass Index; Electroacupuncture; Female; Gonadotropins; Humans; Longitudinal Studies; Ovulation Induction; Polycystic Ovary Syndrome; Prolactin; Prospective Studies; Sex Hormone-Binding Globulin

To investigate the relationship between elevated luteinizing hormone (LH), hyperinsulinemia and neuropeptides in patients with polycystic ovarian syndrome (PCOS).. An oral glucose (100g) tolerance test (OGTT) was performed in 15 normally menstruating women (control) and 30 PCOS women with LH/follicle stimulating hormone (FSH) ratio greater than 3 (group 1) and 25 PCOS subjects with the ratio < 3 (group 2). The responses of insulin, somatostatin (SS), beta-endorphin (beta-EP) and dynorphin A (Dyn A) during OGTT were measured by RIA.. In basal state, significant negative correlations were found between LH and SS (r = -0.51, P < 0.05) in group 1 and between LH and beta-EP (r = -0.49, P < 0.05) in group 2. During OGTT, PCOS women had a greater beta-EP and Dyn A responses in group 1 and an impaired SS response in group 2 as compared with the control.. These data suggested lower endogenous SS, higher beta-EP and Dyn A may lead to elevation of LH and insulin secretions in patients with PCOS.

Topics: Adult; beta-Endorphin; Dynorphins; Female; Follicle Stimulating Hormone; Glucose Tolerance Test; Humans; Insulin; Luteinizing Hormone; Peptide Fragments; Polycystic Ovary Syndrome; Somatostatin

The present study aims to explore whether β-EP in serum (sβ-EP) and follicular fluid (ffβ-EP) could predict the in vitro fertilization (IVF) outcomes of patients with polycystic ovary syndrome (PCOS) and diminished ovarian reserve (DOR).. 90 PCOS women, 50 DOR women, and 100 women with normal ovarian function (control group), who were all undergoing an IVF-embryo transfer trial, were included in the study. Biochemical characteristics, anti-Mullerian hormone (AMH), sβ-EP, ffβ-EP, embryo formation, and pregnancy indicators were assessed in all women. The correlations of AMH and β-EP with oocyte quality were analyzed. Population-based and age-category stratified receiver operating characteristic (ROC) curve analysis of AMH and β-EP for predicting pregnancy and live birth were performed.. Compared with the control group, the PCOS group had higher antral follicle count, testosterone, luteinizing hormone, AMH, sβ-EP, and ffβ-EP, which were lower in the DOR group. Meanwhile, the PCOS and DOR groups had higher cycle cancellation and miscarriage rates, and lower high quality embryo numbers. Correlation analysis showed that the oocyte quality were positively correlated with AMH, sβ-EP, and ffβ-EP. The population-based and age-stratified ROC curve analysis showed that sβ-EP and ffβ-EP had high sensitivity and specificity to predict pregnancy and live birth. Meanwhile, age-stratified AMH enhanced the sensitivity for prediction of live birth after IVF.. sβ-EP and ffβ-EP are different among women with PCOS, DOR, and normal ovarian function. β-EP can be used as a good predictor of clinical pregnancy and live birth after IVF.

Topics: Adult; beta-Endorphin; Female; Fertilization in Vitro; Humans; Ovarian Reserve; Polycystic Ovary Syndrome; Pregnancy; Pregnancy Outcome

To compare the concentrations of beta endorphin in serum and follicular fluid (FF) of PCOS- and non-PCOS women. Secondarily, to investigate associations between beta endorphin and other parameters.. Fifty-nine women undergoing in vitro fertilization (IVF) were included in the study. Sixteen were stratified to the PCOS group using the Rotterdam criteria. The remaining 43 women served as controls. Follicular fluid was collected during oocyte retrieval and peripheral blood sampling was performed on the same day. Beta endorphin concentrations in serum and follicular fluid, serum levels of insulin, glucose, LH, estradiol and progesterone were measured. Additionally, testosterone was measured before starting the stimulation protocol.. There was no difference in beta endorphin levels between PCOS- and non-PCOS women. The concentration of the peptide was higher in serum than in FF, likely due to collection of FF after ovulation induction and corresponding to the early luteal phase. We found a significant correlation between the number of mature Metaphase II (MII) oocytes retrieved and beta endorphin concentration in FF. In women with biochemical hyperandrogenemia, beta endorphin levels in FF correlated with testosterone levels.. Beta Endorphin concentrations in serum and FF do not differ between PCOS- and non PCOS-women undergoing IVF. However, together with sex hormones, beta endorphin might play a key role in oocyte maturation.

Topics: Adult; beta-Endorphin; Female; Follicular Fluid; Humans; Polycystic Ovary Syndrome; Young Adult

Despite some evidence that indicates that the evolution of polycystic ovary syndrome (PCOS) is related to the activity of the endogenous opioid system, and that concentration of plasma β-endorphin levels can increase pain threshold, there are no studies which evaluate pressure pain threshold in the PCOS women population.. In 48 lean women with PCOS and 38 lean women without this disorder plasma β-endorphins and PPT were measured.. The β-endorphins level was higher in the PCOS group compared to the controls (15.28±2.49 pg/mL vs. 6.33±1.71 pg/mL, P<0.001). In PCOS group PPTs measured on deltoid and trapezius muscles were higher compared to the controls (9.33±1.3 kg/cm² vs. 5.19±0.57 kg/cm², P<0.001; 8.23±1.04 kg/cm² vs. 4.79±0.55 kg/cm², P<0.001). The β-endorphin levels positively correlated with PPTs in PCOS group. Increase in β-endorphin level of 1 pg/mL was associated with increase of PPT value on deltoid muscle of 0.23 kg/cm² (R=0.632, P=0.011) and of 0.18 kg/cm² on trapezius muscle (R=0.588, P=0.037). There were no correlations between testosterone level and PPT in PCOS group.. β-endorphin serum level as well as PPT are higher in lean PCOS group than in controls. We found correlations between β-endorphin levels and PPT in the PCOS group. It may suggest the role of endogenous opioids in the pathogenesis of PCOS and also that the increases in circulating plasma β-endorphins concentration can increases PPT in this group.

Topics: Adolescent; Adult; beta-Endorphin; Body Composition; Body Mass Index; Female; Humans; Muscle, Skeletal; Pain Threshold; Polycystic Ovary Syndrome; Young Adult

The evaluation the β-endorphin plasma levels in lean women with polycystic ovary syndrome as well as in women without this disorder. The associations between β-endorphins and other laboratory parameters were also investigated.. 31 women lean, defined as women with normal range body mass index, 15 with polycystic ovary syndrome and 16 without this disorder were included to the study. In all the patients the level of β-endorphins was measured. Also the diagnostic laboratory profile including hormone assessment was made in all patients.. There were significant differences in β-endorphin levels between the 2 groups. The β-endorphin level was higher in the polycystic ovary syndrome group compared to the healthy controls (15.5±4.37 pg/ml vs. 6.9±2.47 pg/ml, p<0.0001). The β-endorphin levels positively correlated with cortisol at 8 am (R=0.632, p=0.011) and negatively correlated with sex hormone binding globuline (R=0.518, p=0.0478) in polycystic ovary syndrome group. Increase in β-endorphin level of 1 pg/ml was associated with an increase of cortisol at 8 am level of 1.134 µg/dl and decrease of sex hormone binding globuline of 0.948 nmol/l in polycystic ovary syndrome group.. Our study showed that the levels of β-endorphins were significantly higher in lean patients with polycystic ovary syndrome than in lean controls. Moreover, β-endorphins levels were found to be correlated with other hormonal parameters. In this respect, β-endorphins may play a role in polycystic ovary syndrome pathophysiology.

Topics: Adult; beta-Endorphin; Body Mass Index; Female; Humans; Polycystic Ovary Syndrome

This pilot study describes a relationship between insulin resistance and μ-opioid neurotransmission in limbic appetite and mood-regulating regions in women with polycystic ovary syndrome (PCOS), suggesting that insulin-opioid interactions may contribute to behavioral and reproductive pathologies of PCOS. We found that [1] patients with PCOS who are insulin-resistant (n = 7) had greater limbic μ-opioid receptor availability (nondisplaceable binding potential) than controls (n = 5); [2] receptor availability was correlated with severity of insulin resistance; and [3] receptor availability normalized after insulin-regulating treatment.

Topics: Adult; beta-Endorphin; Binding Sites; Brain; Carbon Radioisotopes; Case-Control Studies; Female; Fentanyl; Glucose Tolerance Test; Humans; Hypoglycemic Agents; Insulin Resistance; Magnetic Resonance Imaging; Metformin; Michigan; Pilot Projects; Polycystic Ovary Syndrome; Positron-Emission Tomography; Receptors, Opioid, mu; Time Factors; Treatment Outcome; Young Adult

The human endocrinological disorder polycystic ovary syndrome (PCOS) is a common cause of reproductive failure. Even though the cause of PCOS is unknown, hormone and immune disturbances as well as hyperactivity in the sympathetic nervous system are likely to be involved in the pathogenesis of the disease. The present study was undertaken to elucidate if rats with estradiol valerate (EV)-induced polycystic ovaries (PCO) have altered beta-endorphin concentrations in the hypothalamus and in plasma and if they have alterations in circulating immune cell populations and the activity. Repeated low-frequency (2 Hz) electroacupuncture (EA) treatments are known to modulate the release of beta-endorphin, immune responses, and the activity in the autonomic nervous system. We therefore also investigated the effect of EA treatments on the beta-endorphin and the immune systems. Low-frequency EA was given 12 times, 25 min each, over 30 days starting 2-3 days after i.m. injection of EV. The beta-endorphin concentrations in the hypothalamus and in plasma as well as the frequencies of CD4+ T cells and CD8+ T cells were significantly lower in EV-injected control rats as compared to oil-injected control rats. Repeated EA treatments in EV-injected rats significantly increased beta-endorphin concentrations in the hypothalamus. In conclusion, these findings show that both the beta-endorphinergic and the immune system are significantly impaired in rats with steroid-induced PCO and that repeated EA treatments can restore some of these disturbances.

Topics: Animals; Antigens, CD; Antigens, Differentiation, B-Lymphocyte; beta-Endorphin; CD4-CD8 Ratio; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Electroacupuncture; Estradiol; Female; Hypothalamus; Killer Cells, Natural; Macrophages; Monocytes; Polycystic Ovary Syndrome; Rats; Rats, Inbred WKY; Receptors, Transferrin

The aim of this study was to determine the influence of body weight on circulating plasma levels of beta-endorphin and insulin in women with polycystic ovary disease (PCOD), as well as the correlation between the plasma levels of beta-endorphin and insulin. One-hundred and sixty-seven consecutive subjects with PCOD were recruited, 117 of whom had normal weight (body mass index (BMI) < 25) while 50 were obese (BMI > 25). A venous blood sample was taken and plasma concentrations of beta-endorphin, insulin, gonadotropins, prolactin, progesterone, 17 beta-estradiol, estrone, androgens, dehydroepiandrosterone sulfate and sex hormone-binding globulin (SHBG) were measured. Mean beta-endorphin and insulin plasma levels were significantly higher (p < 0.05) in obese PCOD women than in non-obese ones. Correlation analysis showed a positive association between insulin and beta-endorphin, beta-endorphin and BMI (and weight), insulin and BMI (and weight), and a negative correlation was found between insulin and SHBG. A weak association was found between beta-endorphin and luteinizing hormone (LH) in peripheral plasma. Stratified and linear regression analysis showed that plasma beta-endorphin concentrations correlate more with BMI than with insulinemia.

Topics: Adolescent; Adult; beta-Endorphin; Body Mass Index; Case-Control Studies; Female; Hormones; Humans; Insulin; Obesity; Polycystic Ovary Syndrome; Sex Hormone-Binding Globulin

The plasma levels of beta-endorphin were studied in 64 women with polycystic ovarian disease (PCOD), from whom was selected a group of 23 women with normal weight and amenorrhea of < 36 days. On day 21, beta-endorphin levels were: mean 64.92 pg/ml; SD 37.32 pg/ml; 95% CI 48.38-81.47 pg/ml. It was also observed that their levels of opioid peptide were reduced, compared with women who had normal ovulatory cycles, both in the follicular phase (mean 70.93 pg/ml; SD 24.59 pg/ml; 95% CI 76.84-99.77 pg/ml) and luteal phase (mean 88.30 pg/ml; SD 31.80 pg/ml; 95% CI 76.84-99.77 pg/ml). The results were statistically significant (p < 0.05) for levels in PCOD patients compared with those of the luteal phase in women with normal ovulatory cycles. The decreased levels of beta-endorphin were negatively related to luteinizing hormone (LH) levels, which might explain the rise of LH levels in women with PCOD who control their weight and at the time of amenorrhea, although it is not clear if central opioid activity is reflected in the peripheral blood.

Topics: Adolescent; Adult; Amenorrhea; Androstenedione; beta-Endorphin; Body Mass Index; Dehydroepiandrosterone; Estradiol; Female; Follicle Stimulating Hormone; Humans; Immunoenzyme Techniques; Luteinizing Hormone; Menstrual Cycle; Polycystic Ovary Syndrome; Progesterone; Radioimmunoassay; Sex Hormone-Binding Globulin; Testosterone

This article summarizes the studies of the mechanism of electroacupuncture (EA) in the regulation of the abnormal function of hypothalamic-pituitary-ovarian axis (HPOA) in our laboratory. Clinical observation showed that EA with the effective acupoints could cure some anovulatory patients in a highly effective rate and the experimental results suggested that EA might regulate the dysfunction of HPOA in several ways, which means EA could influence some gene expression of brain, thereby, normalizing secretion of some hormones, such as GnRH, LH and E2. The effects of EA might possess a relative specificity on acupoints.

Topics: Adrenal Glands; Animals; Anovulation; beta-Endorphin; Brain; Corticosterone; Electroacupuncture; Epithelial Cells; Estradiol; Female; Gene Expression; Gonadotropin-Releasing Hormone; Hypothalamo-Hypophyseal System; Infertility; Luteinizing Hormone; Ovariectomy; Ovary; Polycystic Ovary Syndrome; Proto-Oncogene Proteins c-fos; Rats; Rats, Wistar; Receptors, Estrogen; RNA, Messenger; Sexual Maturation; Vagina

To investigate the relationship between elevated LH, hyperinsulinemia and neuropeptides in polycystic ovarian syndrome (PCOS), we measured the endogenous levels of insulin, somatostatin (SS), beta-endorphin (beta-EP) and dynorphin A (Dyn A) before and after a glucose load in three groups: group 1 (LH/ FSH > or = 3, n = 30); group 2 (LH/FSH < 3, n = 25), and controls (n = 15). In the basal state, significantly negative correlations were found between LH and SS (r = -0.51, p < 0.05) in group 1 and between LH and beta-EP (r = -0.49, p < 0.05) in group 2. After a glucose load, PCOS women had greater beta-EP and Dyn A responses in group 1 and impaired SS response in group 2 as compared with the control. The data suggest endogenously lower SS, higher beta-EP and Dyn A may contribute to the elevation of LH and insulin secretions in PCOS.

Topics: Adult; beta-Endorphin; Catheterization; Catheters, Indwelling; Cohort Studies; Dynorphins; Female; Glucose; Humans; Insulin; Luteinizing Hormone; Polycystic Ovary Syndrome; Reference Values; Somatostatin; Time Factors

We examined the effects of an oral glucose load on plasma insulin, androgens, and beta-endorphin (beta EP) concentrations in patients carefully selected as having polycystic ovary syndrome (PCOS) and normal glucose tolerance. Our aim was to verify whether insulin resistance is a common feature of PCOS and to differentiate the metabolic abnormalities related to PCOS from those associated with obesity. Plasma immunoreactive insulin (IRI), C-peptide (C-PR), testosterone, androstenedione, dehydroepiandrosterone sulfate, ACTH, and beta EP responses to a 3-h oral glucose tolerance test (OGTT) were evaluated in 10 obese (OB-PCOS) and 10 nonobese (NO-PCOS) patients with PCOS and in 7 obese and 7 nonobese ovulatory controls. OB-PCOS and NO-PCOS did not differ significantly from weight-matched controls in the IRI response, but had a significantly higher C-PR response in terms of mean postglucose load levels and mean incremental areas. During OGTT, mean plasma levels of testosterone, androstenedione, and dehydroepiandrosterone sulfate declined in both PCOS groups as well as in controls, and no significant correlation between the plasma androgen and IRI or C-PR responses was found. The ACTH response in OB-PCOS and NO-PCOS was similar to that in controls, with a progressive decrease until 180 min. A similar decline in plasma beta EP was found in controls, whereas no change in plasma beta EP was observed in OB-PCOS and NO-PCOS. These findings indicate that independently of the presence of obesity, PCOS patients have enhanced insulin secretion in response to OGTT and show a peculiar pattern of changes in plasma beta EP.

Topics: Administration, Oral; Adult; Androgens; Androstenedione; beta-Endorphin; C-Peptide; Dehydroepiandrosterone; Dehydroepiandrosterone Sulfate; Female; Glucose; Glucose Tolerance Test; Humans; Insulin; Insulin Resistance; Obesity; Polycystic Ovary Syndrome; Radioimmunoassay; Testosterone

Polycystic ovary (PCO) syndrome is biochemically characterized by abnormal gonadotropin secretion and polycystic ovaries associated with increase in size and functional activity of stromal tissue; multifollicular ovaries (MFO) are defined by the presence of multiple cysts with no increase in stromal tissue. A central (hypothalamic-pituitary) abnormality, including high plasma beta-endorphin (BE) concentrations without simultaneous elevation of ACTH, was reported for subjects with PCO syndrome. Since we have found the presence of high plasma BE concentrations in hereditary angioedema (HANE) during attacks as well as during symptom-free periods, we studied, by means of pelvic ultrasound scanning employed to determine the prevalence of PCO and of MFO, 13 women of reproductive age affected with HANE who were not on oral contraceptives. We have found PCO in 5/13 (38.4%) and MFO in 7/13 (53.8%) HANE patients. Nine patients had oligomenorrhoea (five with PCO, three with MFO, one with normal ovaries), five (three with PCO, two with MFO) were hirsute and only one (with MFO) had weight loss. No patient was obese. Mean plasma LH, testosterone, prolactin, cortisol and ACTH concentrations were normal, while FSH was significantly reduced and LH/FSH ratio increased. BE concentrations were significantly high in all the patients studied. Our results clearly demonstrate that women with HANE frequently have cystic ovaries (polycystic or multifollicular) in the presence of high BE concentrations.

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Angioedema; beta-Endorphin; Female; Humans; Hydrocortisone; Oligomenorrhea; Ovarian Cysts; Pelvis; Polycystic Ovary Syndrome; Prevalence; Prolactin; Reference Values; Testosterone; Ultrasonography

Our purpose was to investigate the source and role of elevated levels of immunoreactive beta-endorphin in polycystic ovary syndrome. We wished to determine whether immunoreactive beta-endorphin secretion in patients with polycystic ovary syndrome is influenced by body weight and whether the pituitary release of immunoreactive beta-endorphin with corticotropin-releasing hormone is related to luteinizing hormone levels or adrenal androgen secretion.. Eighteen patients with polycystic ovary syndrome and 10 ovulatory controls were studied. Each subject received 1 microgram/kg intravenous corticotropin-releasing hormone and an oral glucose tolerance test on alternate days. Levels of plasma immunoreactive beta-endorphin, corticotropin, luteinizing hormone, cortisol, adrenal androgens, and insulin were measured.. Although immunoreactive beta-endorphin levels were elevated in patients with polycystic ovary syndrome (p < 0.01), incremental responses after corticotropin-releasing hormone were similar to controls and were not influenced by body weight. Serum luteinizing hormone levels were not affected by corticotropin-releasing hormone and did not correlate with immunoreactive beta-endorphin levels. Adrenal androgen responses after corticotropin-releasing hormone were increased in patients with polycystic ovary syndrome (p < 0.01) but were not correlated with immunoreactive beta-endorphin secretion. After oral glucose was given, elevated fasting insulin levels increased significantly in patients with polycystic ovary syndrome (p < 0.01), as did immunoreactive beta-endorphin levels (p < 0.05). The increases in insulin and immunoreactive beta-endorphin levels were correlated (p < 0.05).. Pituitary secretion of immunoreactive beta-endorphin is normal in patients with polycystic ovary syndrome, and pancreatic secretion appears to be increased. Corticotropin-releasing hormone does not influence luteinizing hormone levels, and adrenal androgen sensitivity is not influenced by immunoreactive beta-endorphin secretion.

Topics: Adult; beta-Endorphin; Corticotropin-Releasing Hormone; Female; Glucose Tolerance Test; Humans; Luteinizing Hormone; Pituitary Gland; Polycystic Ovary Syndrome; Radioimmunoassay; Reference Values

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.

Topics: Animals; Autoradiography; beta-Endorphin; D-Ala(2),MePhe(4),Met(0)-ol-enkephalin; Drug Implants; Estradiol; Female; Hypothalamus; Iodine Radioisotopes; Organ Specificity; Polycystic Ovary Syndrome; Rats; Receptors, Opioid; Receptors, Opioid, delta; Receptors, Opioid, kappa; Receptors, Opioid, mu

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.

Topics: Adolescent; Adult; beta-Endorphin; Female; Follicle Stimulating Hormone; Humans; Luteinizing Hormone; Obesity; Polycystic Ovary Syndrome; Sex Hormone-Binding Globulin

Increased responses of plasma insulin and endorphins to the oral glucose tolerance test (oGTT) have earlier been found in obese women. We studied responses of immunoreactive beta-endorphin (ir beta-E) and insulin in plasma to the oGTT in 8 non-obese women with polycystic ovaries (PCO) and in 10 healthy women. An additional control group consisted of 5 healthy women who were fasting during the study period. In the PCO group the insulin and glucose responses to the oGTT were increased, and an increase of ir beta-E from 5.9 +/- 1.5 to 8.6 +/- 2.8 pmol/l was found during the 1st half-hour period of the oGTT. In contrast, no significant change was found during the oGTT in healthy women (3.2 +/- 0.5 and 2.7 +/- 0.65 pmol/l, respectively), and in the fasting control women the mean ir beta-E level (+/- SE) decreased, from 4.5 +/- 1.2 to 3.6 +/- 1.1 pmol/l. These findings revealed increased responses of both plasma ir beta-E and insulin to the oGTT in non-obese women with PCO but their possible causal relationship remained unsolved.

Topics: Adult; beta-Endorphin; Body Weight; Female; Glucose Tolerance Test; Humans; Insulin; Polycystic Ovary Syndrome

Topics: beta-Endorphin; Female; Humans; Ovarian Follicle; Polycystic Ovary Syndrome

The possibility of local ovarian production of beta-endorphin prompted us to measure beta-endorphin levels in 19 follicular fluid samples obtained from normal ovaries and compare them with beta-endorphin plasma levels in 19 women with normal ovulation. beta-Endorphin was extracted through Sepharose-treated chromatography columns and assayed with a specific anti-beta-endorphin antibody. Follicular fluid beta-endorphin levels (21.3 +/- 10.8 pg/ml) were significantly higher (p less than 0.01) than the plasma levels (15.5 +/- 3.35 pg/ml). There was no significant correlation between plasma and follicular fluid beta-endorphin concentrations. Follicles greater than 1 cm in size contained more beta-endorphin than follicles less than 1 cm in size (22.7 +/- 3.5 versus 18.7 +/- 4.4 pg/ml, p less than 0.05). Five follicular fluid samples were obtained from polycystic ovaries. The mean beta-endorphin content (45.1 +/- 7.7 pg/ml) in these follicles was significantly higher than that of normal ovaries (p = 0.001). It is concluded that the ovaries produce beta-endorphin and that polycystic ovaries produce more beta-endorphin than normal ovaries.

Topics: beta-Endorphin; Endorphins; Female; Humans; Ovarian Follicle; Ovary; Polycystic Ovary Syndrome

Topics: Adult; beta-Endorphin; Female; Humans; Immunoenzyme Techniques; Ovary; Polycystic Ovary Syndrome

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.

Topics: Adrenocorticotropic Hormone; Adult; beta-Endorphin; beta-Lipotropin; Endorphins; Female; Humans; Polycystic Ovary Syndrome

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.

Topics: Adolescent; Adult; Androgens; beta-Endorphin; Body Composition; Endorphins; Female; Hirsutism; Humans; Middle Aged; Obesity; Polycystic Ovary Syndrome

The inhibitory role of the dopaminergic and opioidergic mechanisms in the control of LH secretion in patients with polycystic ovary syndrome (PCO) was evaluated. The administration of an opiate receptor antagonist, naloxone, of a dopamine receptor antagonist, metoclopramide, or of human synthetic beta h-endorphin, were unable to alter LH secretory activity in patients with PCO. Since identical doses of these antagonists and the opiate agonist have elicited respectively a rise and fall of LH levels in normal cycling women, these findings suggest that an underlying hypothalamic component of defect in endogenous dopamine and opioid control may be responsible for the inappropriate gonadotrophin secretion in this syndrome.

Topics: beta-Endorphin; Depression, Chemical; Endorphins; Female; Humans; Hypothalamus; Luteinizing Hormone; Metoclopramide; Naloxone; Polycystic Ovary Syndrome

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.

Topics: Adolescent; Adult; Amenorrhea; beta-Endorphin; Body Weight; Endorphins; Female; Follicle Stimulating Hormone; Humans; Luteinizing Hormone; Polycystic Ovary Syndrome; Radioimmunoassay

The authors have suggested that dysfunction of a central structure (above the pituitary level) is the primary etiologic factor responsible for the production of the polycystic ovary syndrome. To investigate further the functional integrity of the hypothalamic pituitary axis, plasma levels of beta-endorphin, gamma 3-melanocyte stimulating hormone, and gamma 1-melanocyte stimulating hormone-like immunoreactivity were measured in six patients with polycystic ovary syndrome, and in ten women with normal ovarian function. The limit of sensitivity for the radioimmunoassays was 20 pg/mL. Plasma beta-endorphin was significantly higher in polycystic ovary syndrome than in control subjects: (mean +/- SE) 60 +/- 10 versus 30 +/- 4 pg/mL, respectively (P less than .05). gamma 3-Melanocyte stimulating hormone was detectable in four of six patients with polycystic ovary syndrome (mean for the whole group: 45 +/- 15 pg/mL); it was undetectable in all the control subjects. Control of plasma beta-endorphin and gamma 3-melanocyte stimulating hormone secretion in PCO was evaluated with metyrapone and dexamethasone. Overnight administration of metyrapone to polycystic ovary syndrome patients resulted in rises of beta-endorphin and gamma 3-melanocyte stimulating hormone. Dexamethasone suppressed only partially (to basal concentrations) beta-endorphin and gamma 3-melanocyte stimulating hormone levels. Plasma adrenocorticotropic hormone concentrations were within the normal range and displayed the expected changes in response to metyrapone and dexamethasone. The present report presents an additional central (hypothalamic-pituitary) abnormality in patients with the polycystic ovary syndrome.

Topics: Adrenocorticotropic Hormone; Adult; beta-Endorphin; Dexamethasone; Endorphins; Female; Humans; Hydrocortisone; Melanocyte-Stimulating Hormones; Metyrapone; Polycystic Ovary Syndrome; Radioimmunoassay