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 association between plasma calcitonin and beta-endorphin has been shown in various studies with analgesic and thermoregulatory effects. In the present study, we sought a similar association between those chemicals and physiological menopausal hot flush. Plasma calcitonin and beta-endorphin levels were measured in 5 women in physiologic menopause who suffered from frequent episodes of hot flushes. An increase in plasma calcitonin levels was noted during the hot flushes, although it was not significant. In contrast, plasma beta-endorphin levels fell significantly at onset of the hot flush, as compared to their levels 5-20 min earlier (p less than 0.005), and rose 5-15 min following the hot flush episode.
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PMID:Menopausal hot flushes, plasma calcitonin and beta-endorphin. A preliminary report. 155 34

Endocrinological studies on stressed climacteric women and some cases of gonadal dysfunction were carried out by analysing blood levels of adrenocorticotropic hormone (ACTH), beta-lipotropin (beta-LPH) and beta-endorphin (beta-EP) after the administration of synthetic corticotropin releasing factor (CRF, CRF test). Our results can be summarized as follows: 1. The responsiveness to CRF in perimenopausal and ovariectomized women rose and it corresponded with those of post gonadectomy in testicular feminization. 2. Responsiveness to CRF was decreased as estrogen levels decreased with the patient's age, and a similar tendency was observed in gonadal dysfunction. 3. Climacteric women with non-specific complaints have a higher responsiveness to CRF than that of postmenopausal women without complaints. Subjects with a high K.I score and with severe hot flush showed higher responsiveness to CRF than other subjects. These data suggest that CRF and its related hormones may be correlative with stress and hot flushes in climacteric periods and endogenous CRF may play an important psychosomatic role by regulating the hypothalamo-pituitary-adrenal function where there is decreased estrogen.
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PMID:[Endocrinological analysis of climacteric symptoms and gonadal dysfunction by CRF test]. 216 10

Hot flushes are not caused by hypergonadotrophinaemia. This is apparent because peaks of gonadotrophin in the serum do not coincide with cutaneously measured hot flushes while such flushes still occur in hypophysectomized women. Gonadotrophin-releasing hormone and other neurotransmitters (possibly beta-endorphin) affect thermoregulation. The following hypothesis is advanced. During the climacteric period neurotransmitter changes, a decrease in catechol oestrogens, a decrease in alpha-2-adrenoceptor activity and cessation of ovarian steroid production may lead to alterations in endogenous opiate activity and thus to disturbances of thermoregulation, resulting in the occurrence of hot flushes. Low beta-endorphin levels in the peripheral plasma, which rise again following oestrogen treatment, are observed during the climacteric. On the other hand, women with severe hot flushes caused by a stress event show enormously increased beta-endorphin values, which are normalized by hormone substitution therapy acting via still unknown neuroendocrinological feedback mechanisms.
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PMID:Beta-endorphin levels during the climacteric period. 284 May 57

The present study shows the effects of two different steroid replacement therapies, with conjugated estrogens or with a new synthetic steroid derivative, ORG OD14, on plasma beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) levels in postmenopausal subjects. Blood samples were collected before treatment and after 1, 2 and 4 months of treatment; a third group of patients was treated with placebo. After 2 months of treatment both groups of patients who underwent steroid supplementation showed circulating levels of beta-EP and beta-LPH higher than basal levels. ORG OD14 treatment increased beta-EP and beta-LPH levels more than conjugated estrogens at the 2nd month of therapy. No further change was found after 4 months. The two drugs were effective in reducing hot flushes and improving physical and psychological symptoms. These data indicate that sex steroids are able to increase beta-EP and beta-LPH secretion in postmenopausal women, with a concomitant relief of climacteric symptoms.
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PMID:Steroid replacement treatment increases beta-endorphin and beta-lipotropin plasma levels in postmenopausal women. 285 6

Plasma beta-endorphin levels were measured in five women in physiologic menopause suffering from frequent episodes of hot flushes, recorded objectively by the measurement of finger temperature. Significantly lower levels of plasma beta-endorphin levels were found at the onset of the hot flushes than five to 20 minutes before (P less than .001). After the flush there was a significant rise of plasma beta-endorphin levels at five, ten, and 15 minutes (P less than .002).
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PMID:Menopausal hot flushes and plasma beta-endorphins. 295 61

The present study reports the plasma levels of gonadotropins (luteinizing hormone, follicle-stimulating hormone), proopiomelanocortin-related peptides (adrenocorticotropic hormone, beta-endorphin, and beta-lipotropin), and cortisol in eight menopausal women experiencing frequent hot flushes. beta-Endorphin and beta-lipotropin levels were measured by radioimmunoassay after extraction and Sephadex G-75 column chromatography. Plasma levels of adrenocorticotropic hormone (after extraction), luteinizing hormone, follicle-stimulating hormone, and cortisol were measured by specific radioimmunoassay. All hormone levels showed a prompt and significant rise on occurrence of hot flushes (18 total recordings), remained high for 15 minutes, and decreased to basal levels 35 minutes later. The evaluation of the behavior pattern of single hormone levels revealed a more pronounced increase of proopiomelanocortin-related peptides and cortisol than of gonadotropins (p less than 0.01).
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PMID:Increase of proopiomelanocortin-related peptides during subjective menopausal flushes. 608 64

Eighteen postmenopausal women with severe hot flashes had continuous recordings of finger temperature and skin resistance as objective indexes of flushing episodes, and serial measurements of anterior pituitary hormones as indirect indexes of hypothalamic neurotransmitter activity. Significant increases of growth hormone, adrenocorticotropic hormone (ACTH), and luteinizing hormone (LH) occurred with maximal concentrations at 30, five, and 15 minutes, respectively, after the onset of the skin temperature rises. No significant fluctuations of prolactin (PRL), thyroid-stimulating hormone (TSH), or follicle-stimulating hormone (FSH) were observed. The mean serum cortisol concentration increased 15 minutes after the hot flash, presumably consequent to the preceding elevation of ACTH. Pituitary ACTH release may be secondary to hypothalamic cooling, whereas increased growth hormone and LH output and the thermoregulatory adjustments comprising the flushing episodes are all consistent with cyclic episodes of increased hypothalamic norepinephrine activity.
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PMID:Pituitary hormones during the menopausal hot flash. 609 54