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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Plasma beta-endorphin levels in obese and non-obese patients with polycystic ovary disease. 1129 19

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

The object of this study was to examine changes in muscular strength, power, and resting hormonal concentrations during 6 weeks of detraining (DTR) in recreationally strength-trained men. Each subject was randomly assigned to either a DTR (n = 9) or resistance training (RT; n = 7) group after being matched for strength, body size, and training experience. Muscular strength and power testing, anthropometry, and blood sampling were performed before the experimental period (T1), after 3 weeks (T2), and after the 6-week experimental period (T3). One-repetition maximum (1RM) shoulder and bench press increased in RT at T3 (p </= 0.05), whereas no significant changes were observed in DTR. Peak power output and mean power output significantly decreased (9 and 10%) in DTR at T2. Peak torque of the elbow flexors at 90 degrees did not change in the RT group but did significantly decrease by 11.9% at T3 compared with T1 in the DTR group. Vertical jump height increased in RT at T2 but did not change in DTR. Neither group displayed any changes in 1RM squat, body mass, percent body fat, or resting concentrations of growth hormone, follicle-stimulating hormone, luteinizing hormone, sex hormone-binding globulin, testosterone, cortisol, or adrenocorticotropin. These data demonstrate that 6 weeks of resistance DTR in recreationally trained men affects power more than it does strength without any accompanying changes in resting hormonal concentrations. For the recreational weight trainer, losses in strength over 6 weeks are less of a concern compared with anaerobic power and upper arm isometric force production. Anaerobic power exercise with a high metabolic component coming from glycolysis might be of importance for reducing the impact of DTR on Wingate power performances. A minimal maintenance training program is recommended for the recreational lifter to offset any reductions in performance.
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PMID:Detraining produces minimal changes in physical performance and hormonal variables in recreationally strength-trained men. 1217 51

Studies in our laboratory and elsewhere have demonstrated numerous abnormalities of steroid and polypeptide hormone secretion in obesity: hyperestrogenemia and hypogonadotropic hypogonadism in obese men; diminished SHBG levels in both sexes; elevated free testosterone and free estradiol in obese women; PCOS-like gonadotropin and sex-hormone abnormalities in obese women; elevated serum insulin in both sexes; blunted stimulability of prolactin, growth hormone, and vasopressin in both sexes; and elevated basal levels and blunted stimulability and suppressibility of beta-endorphin in both sexes. All of these abnormalities have been clearly shown to be partly or completely reversible with weight loss, with the exception of the endorphin abnormalities. In that area, four out of the five studies reported show no reversibility with weight loss. Reversibility of nearly all the hormonal abnormalities of obesity (i.e., all but the hyperendorphinemia) by weight loss suggests that none of them is causative of obesity. Nevertheless, some of the reversible abnormalities may secondarily amplify the morbidity associated with obesity: the hyperinsulinemia may be related to the increased risk of hypertension, hyperlipidemia, coronary disease, and Type II diabetes; the elevated levels of free estradiol in obese women may be related to their increased risk of breast and endometrial cancer. The role of hyperendorphinemia in obesity clearly requires further investigation, since it is the only observed hormonal abnormality that appears to be non-reversible by weight loss, and also since there seems to be increased sensitivity to beta-endorphin in obesity. The possibility that endorphin abnormalities may be causal in obesity cannot be ruled out.
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PMID:A perspective on the hormonal abnormalities of obesity: are they cause or effect? 1635 9

Dehydroepiandrosterone (DHEA) is commonly used by HIV-infected men, but its endocrine effects in this population are not well defined. We conducted an 8-week randomized, placebo-controlled trial to determine the effects of escalating doses (100-400 mg/d) of DHEA on the hypothalamic-pituitary-adrenal and hypothalamic-pituitary-gonadal axes, and on a number of metabolic parameters in 69 HIV-positive men (31 in DHEA-treated group, 38 in placebo group). High-dose (250 microg) corticotropin and luteinizing hormone-releasing hormone stimulation tests were carried out in all subjects. Fifty-four subjects (26 in the DHEA-treated group and 28 in the placebo group) also underwent optional corticotropin-releasing hormone test, and 67 subjects (31 in DHEA-treated group and 36 in placebo group) underwent optional low-dose (1 microg) corticotropin stimulation test. All tests were performed at baseline and at the end of week 8. Repeated-measures analysis of variance was used to analyze the data. We observed significant increases in circulating levels of DHEA, DHEA-sulfate, free testosterone, dihydrotestosterone, androstenedione, and estrone, and a decline in the serum concentration of sex hormone-binding globulin in the DHEA-treated group but not in the placebo group (P < .001). There were no differences between the groups in other endocrine or metabolic parameters or in the results of the stimulation tests. In conclusion, oral DHEA therapy in HIV-positive men significantly increases circulating levels of DHEA and DHEA-sulfate, free testosterone, dihydrotestosterone, androstenedione, and estrone and suppresses circulating concentration of sex hormone-binding globulin. Long-term studies are needed to assess the clinical significance of these hormonal changes in subjects with HIV infection receiving oral DHEA therapy.
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PMID:Endocrine effects of oral dehydroepiandrosterone in men with HIV infection: a prospective, randomized, double-blind, placebo-controlled trial. 1678 56

The purpose of this study was to evaluate the effects on hormonal milieu of 1-year therapy with 10 mg/day oral dehydroepiandrosterone (DHEA) or 50 microg transdermal estradiol plus 100 mg/day oral micronized progesterone in a group of 20 healthy postmenopausal women (age=50-58 and years since menopause (ysm)=1-6) and also the effects observed by combining these two therapies in a group of 12 postmenopausal women (age=54-61 and ysm=6-10) characterized by lower baseline DHEA and DHEAS levels (<2.40 and <0.55 microg/ml, respectively). DHEA produced a significant rise in androgens levels, whereas HRT did not. Moreover, DHEA alone induced a significantly lower increase in estrogens and beta-endorphin levels and a higher decrease in cortisol levels than HRT. DHEA and HRT also produced a significant similar increase in allopregnanolone levels. DHEA plus HRT induced a significantly higher increase in testosterone and estradiol and a lower increase in allopregnanolone and beta-endorphin levels and a significantly lower decrease in cortisol levels than HRT alone treated group. A similar increase was observed in progesterone and SHBG levels in all groups. These results suggest that 10-mg DHEA seems to be the proper dose to replace androgen deficiency in subjects with reduced Delta-5 androgens plasma levels. However, the aging process and the number of years since menopause may further modulate the effects of hormone therapy on hormonal milieu.
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PMID:One-year therapy with 10mg/day DHEA alone or in combination with HRT in postmenopausal women: effects on hormonal milieu. 1839 29

It is well known that acute psychosocial stress activates the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS). However, the effect of acute psychosocial stress on the hypothalamic-pituitary-gonadal (HPG) axis and levels of sex steroids are less known. The aim of this study was to investigate the effect of acute psychosocial stress on serum concentrations of sex steroids in healthy men and women. Twenty men and 19 women (age 30-50 years) underwent Trier Social Stress Test (TSST), a tool for investigating psychobiological stress responses in a laboratory setting. Blood samples were collected before, directly after the stress test, and after 30 min of recovery. Concentrations of androgens were measured with high specificity LC-MS/MS method; concentrations of cortisol, estradiol and sex hormone-binding globulin were determined using immunoassays. In both men and women we observed significantly elevated levels of testosterone, estradiol, androstenedione and sex hormone binding globulin along with significantly increased adrenocorticotropic hormone (ACTH), serum cortisol, heart rate, systolic blood pressure (SBP), and diastolic blood pressure (DBP) as a response to the stressor. Thus, even though the HPG axis and the production of sex steroids may be inhibited during prolonged periods of stress, the sex steroid levels may increase in the initial phase of acute psychosocial stress.
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PMID:Sex steroid levels temporarily increase in response to acute psychosocial stress in healthy men and women. 2240 91


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