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)

1. Forty six women presenting with symptoms of premenstrual syndrome (PMS) were studied. Ages ranged from 21 to 32. All women answered a questionnaire based on DSM-III-R criteria. They then had serum beta-endorphin levels drawn on day 1 and day 20 of their menstrual Cycle. 2. Beta-endorphin levels were compared with symptom presentation. Such symptoms as anxiety, food cravings and physical discomfort were associated with significant decline in beta-endorphin. Other symptoms were found equally distributed in both groups. The existence or absence of beta-endorphin decline in specific PMS subgroup was postulated.
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PMID:Symptoms of premenstrual syndrome as a function of beta-endorphin: two subtypes. 820 81

The results of long-acting, injectible gonadotropin releasing hormone agonist (GnRH-a) and placebo treatment of severe premenstrual syndrome (PMS) patients with regular menstrual cycles and without known psychiatric disorders are reported. Diagnosis was made according to the Menstrual Symptom Questionnaire and Menstrual Symptom Diary scores. In a placebo-controlled, crossover study, 12 subjects were given either normal saline or depot leuprolide acetate (7.5 mg) every 30 days, starting with the onset of menses. Each subject received the same agent twice before switching to the other and did not known which agent was given. A significant decrease in PMS symptoms was reported by all subjects in both treatment regimens. Biweekly venous blood sampling showed significant elevations of beta-endorphin levels and suppression of gonadotropin concentrations in subjects receiving depot leuprolide treatment. Short-term treatment of severe PMS with an injectible, long-acting GnRH-a may not treat the disease more than do saline injections in a group of women selected by certain criteria.
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PMID:Premenstrual syndrome and related hormonal changes. Long-acting gonadotropin releasing hormone agonist treatment. 827 82

Premenstrual syndrome (PMS) is a menstrual cycle-related disorder of mood and behavior with unknown etiology and lack of evidence of endocrine imbalances. The absence of menstrual cyclicity eliminates PMS symptoms, and cyclic gonadal changes appear necessary but not sufficient cause for behavioral symptoms in predisposed women. As there are many depressive symptoms in PMS, we focused on the neuroendocrine characteristics of depression, primarily hypothalamic-pituitary-adrenal hyperactivity, and investigated plasma adrenocorticotropin (ACTH) and cortisol levels in the menstrual cycle. Blood samples were drawn daily from ten patients with PMS and eight asymptomatic control subjects who also reported symptoms daily throughout one menstrual cycle. The ACTH levels were significantly lower in patients with PMS compared to control subjects in the luteal phase. Two PMS subgroups were identified by cluster analysis applied to symptom scores. Plasma ACTH levels of PMS Cluster 1 subjects were significantly lower compared to controls. The ACTH levels of PMS Cluster 2 subjects were nearly identical to controls. These preliminary results suggest distinct hormonal subgroups in the heterogeneous PMS population and support further study of ACTH as a biological correlate of PMS.
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PMID:Preliminary evidence for plasma adrenocorticotropin levels as biological correlates of premenstrual symptoms. 839 59

There are three classes of endogenous opioid peptides: endorphins, enkephalins, dynorphins. Beta-endorphin is the main representative of endogenous opioid peptides. Beta-endorphin plays a role in the regulation of the normal menstrual cycle and possibly in the onset of puberty. This peptide is also involved in the pathophysiology of such menstrual disorders as: exercise-associated amenorrhoea, stress-induced amenorrhoea, weight loss related amenorrhoea and premenstrual syndrome. Probable mechanism is that alterations in the levels of beta-endorphin may change the pulsatile release of GnRH. This article reviews contemporary views on the role of beta-endorphin in the physiology and disorders of the menstrual cycle.
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PMID:[Beta-endorphin--physiologic role and menstrual cycle disorders]. 868 45

Because of the unique combination of physical (e.g. bloating, water retention) and psychological (e.g. mood, memory) symptoms associated with premenstrual syndrome (PMS), various hypothalamic and pituitary hormones have been implicated in the pathophysiology of PMS. We measured plasma adrenocorticotropic hormone (ACTH), arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) across the menstrual cycle in 19 women with PMS and 12 normal women. AVP concentrations were lower throughout the menstrual cycle in symptomatic PMS patients compared with PMS patients during asymptomatic cycles and normal women. No differences in ACTH and ANP were observed between patients and controls. However, ACTH and ANP were positively and significantly correlated with each other in women with PMS but not in controls. These findings contribute to a growing list of menstrual cycle-independent findings in women with PMS and suggest that there may be an underlying neurobiological vulnerability that predisposes some women to experience somatic and mood dysregulation in the luteal phase of the menstrual cycle.
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PMID:Peripheral measures of arginine vasopressin, atrial natriuretic peptide and adrenocorticotropic hormone in premenstrual syndrome. 881 32

Central nervous system hormones have been linked to premenstrual syndrome (PMS) and beta-endorphin (beta-EP) is thought to be involved in the pathophysiology. We have tested the efficacy of the synthetic steroid Org OD 14 (tibolone) in the treatment of PMS. This prospective, randomized, placebo-controlled, double-blind cross-over study included 18 ovulatory women with PMS as ascertained by a visual linear analogue scale (VLAS). The women in each group received either 2.5 mg per day Org OD 14 (n = 9) or a multi-vitamin pill as placebo (n = 9) for 3 months. Treatments were then crossed over to a placebo for a further 3 months. VLAS ratings were evaluated at the end of each menstrual cycle throughout the study. Peripheral beta-EP concentrations were determined by radioimmunoassay on days 7 and 25 of each menstrual cycle. Changes in VLAS score and beta-EP concentrations from baseline were calculated and analysed by Student's paired t-test. Improvements in VLAS scores and beta-EP concentrations were evident during the second and third months of tibolone treatment. At the end of the third month, there was a significant improvement in VLAS scores of all symptom categories compared with pretreatment and placebo during treatment with tibolone (P < 0.05). Similar results were obtained in the first placebo group when switched to tibolone. Beta-EP concentrations were not significantly different between the study groups at the initial cycle (15.9 +/- 3.6 versus 17.2 +/- 2.3 pg/ml). The increase in beta-EP concentration was significantly greater on day 25 of the menstrual cycle in women treated with tibolone compared with baseline and placebo group (22.5 +/- 4.4 versus 15.9 +/- 3.6 and 17.2 +/- 2.3 pg/ml respectively, P < 0.05). Our data confirm the clinical efficacy of tibolone in PMS-related symptoms, as well as its effects on serum beta-EP concentrations in patients with PMS.
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PMID:Placebo-controlled cross-over study of effects of tibolone on premenstrual symptoms and peripheral beta-endorphin concentrations in premenstrual syndrome. 980 57

Estradiol, progesterone and some of their metabolites modulate the activity of neurotransmitters and neuropeptides in the CNS. The distribution and concentrations of sex steroids in the various CNS regions is partly dependent on the serum levels, but also on the local synthesis of the steroids. In general, estradiol and testosterone exert a stimulatory, progesterone an inhibitory effect on neuronal activities which are mediated by excitatory (e.g. glutamate, aspartate), and inhibitory amino acids (e.g. GABA) and neuropeptides (e.g. beta-endorphin), respectively. Gonadotropin release is primarily governed by the rhythm of pulsatile secretion of GnRH in the hypothalamus which is controlled by estradiol and progesterone by means of inhibitory or stimulatory modulation of the amplitude and frequency of GnRH pulses. The discharges of GnRH neurons triggered by excitatory amino acids are modulated by estradiol, while the inhibitory effect of progesterone is mediated by GABA and beta-endorphin which cause hyperpolarization of the GnRH neurons and consequently a reduced pulse frequency. The pulse amplitudes are primarily influenced by estradiol, but neuropeptide Y, neurotensin and noradrenaline contribute to their preovulatory enhancement. The postovulatory rise in core temperature is caused by the increasing level of progesterone and its metabolite 3 alpha-pregnanolone, respectively. Despite of this, up to 20% of ovulatory cycles do not show any rise in body temperature. Although 3 alpha-pregnanolone has sedative activities, there is no change in sleep quality during the luteal phase due to their low serum levels. It could be demonstrated that performance on tests of articulatory and fine motor skills are enhanced in the late follicular phase as compared to the menstruation phase, while spatial ability was better during menses. Estrogens may influence mood and well-being in a favorable manner, while in predisposed women progesterone may cause symptoms of premenstrual syndrome. In most women there are, however, no cycle-dependent mood changes. An increase in appetite can be observed during the periovulatory phase and before menses, while sexual interest increases in the follicular phase. Somatic complaints (back pain, abdominal pain, breast tenderness) which are highest before and during menstruation, are probably associated with a lowered pain threshold due to a fall in the beta-endorphin levels in the CNS.
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PMID:[Influence of the ovarian cycle on the central nervous system]. 1201 35

Several studies have been performed during recent years to investigate the existence of a possible endocrine cause for premenstrual syndrome (PMS); the results reported are often discordant. Great interest has been raised around allopregnanolone, which could be involved in the determination of mood disorders reported by PMS patients. During the luteal phase, lower levels of this hormone have been detected in PMS patients. The aim of our study was to evaluate estradiol, progesterone, dehydroepiandrosterone (DHEA), DHEA sulfate (DHEAS), androstenedione, total and free testosterone, cortisol, pregnenolone and allopregnanolone levels in 20 patients suffering from PMS and to compare them with those found in 20 fertile healthy women in the follicular and the luteal phases. Adrenocorticotropic hormone (ACTH) tests after dexamethasone suppression were performed in 10 patients of each group during the follicular and the luteal phases. In the PMS group, significantly lower allopregnolone levels were found in the luteal phase, while progesterone was lower in the PMS group in both phases. In the PMS group, higher free testosterone levels were found during the luteal phase and higher DHEA levels in both the follicular and the luteal phases. The present data confirm reduced allopregnanolone levels in the luteal phase in PMS patients, together with higher levels of DHEA and free testosterone. It is possible to conclude that, in addition to the previously described reduced luteal secretion of allopregnanolone, the adrenal gland production of this steroid in PMS sufferers is also impaired in the luteal phase. Considering the specific actions of these hormones on the control of mood and behavior, this specific hormonal milieu may contribute to the cyclic occurrence of anxiety, aggressiveness and irritability reported by PMS patients.
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PMID:Adrenal response to adrenocorticotropic hormone stimulation in patients with premenstrual syndrome. 1519 99


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