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)

Earlier observations in our laboratory indicated that i.v. infusion of human/rat corticotropin-releasing hormone (hCRH) suppresses pulsatile luteinizing hormone (LH) and follicle-stimulating hormone (FSH) release in ovariectomized rhesus monkeys. Since cortisol secretion increased significantly as well, it was not possible to exclude the possibility that this inhibitory effect of hCRH on gonadotropins was related to the activation of the pituitary/adrenal axis. The purpose of the present study was to determine the role of pituitary/adrenal activation in the effect of hCRH on LH and FSH secretion. We compared the effects of 5-h i.v. infusions of hCRH (100 micrograms/h, n = 7) and of human adrenocorticotropic hormone (ACTH) (1-24) (5 micrograms/h, n = 3; 10 micrograms/h, n = 3, 20 micrograms/h, n = 3) to ovariectomized monkeys on LH, FSH, and cortisol secretion. As expected, during the 5-h ACTH infusions, cortisol levels increased by 176-215% of baseline control, an increase similar to that observed after CRH infusion (184%). However, in contrast to the inhibitory effect observed during the CRH infusion, LH and FSH continued to be released in a pulsatile fashion during the ACTH infusions, and no decreases in gonadotropin secretion were observed. The results indicated that increases in ACTH and cortisol did not affect LH and FSH secretion and allowed us to conclude that the rapid inhibitory effect of CRH on LH and FSH pulsatile release was not mediated by activation of the pituitary/adrenal axis.
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PMID:The inhibitory action of corticotropin-releasing hormone on gonadotropin secretion in the ovariectomized rhesus monkey is not mediated by adrenocorticotropic hormone. 284 Sep 81

Daily serum immunoreactive beta-endorphin (IR-beta-EP) levels, in conjunction with luteinizing hormone, follicle-stimulating hormone, 17 beta-oestradiol, progesterone, and prolactin, were measured during the ovulatory cycle in five healthy Chinese women. Standardization of raw data by conversion to the statistical "Z scores" and composite plot of the five cycles showed that serum IR-beta-EP levels fluctuated during the follicular, late luteal, and menstrual phases. A preovulatory rise occurred two to three days prior to the luteinizing hormone surge, followed by a postovulatory dip for two to three days. The concentrations of IR-beta-EP were (mean +/- S.E.M.): 85.5 +/- 10.5 pg/mL (n = 36) in the follicular phase; 92.4 +/- 36.5 pg/mL (n = 5) in the ovulatory phase; 72.3 +/- 16.6 pg/mL (n = 7) in the early luteal phase; 100.0 +/- 10.7 pg/mL (n = 38) in the late luteal phase. The values in the luteal phase were the highest of any in the ovulatory cycle. The findings suggest that the fluctuation of endogenous beta-EP is under the influence of, among other factors, ovarian sex steroids. The significance of beta-EP in the regulation of gonadotropin release during normal menstrual cycles is discussed.
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PMID:Serum immunoreactive beta-endorphin in the human ovulatory cycle. 288 43

During 2 hours of bed rest, plasma samples were taken at 15-minute intervals from nine women with exercise-associated amenorrhea and in 11 control women in the follicular phase of a normal menstrual cycle. Concentrations of immunoreactive beta-endorphin, cortisol, prolactin, luteinizing hormone, follicle-stimulating hormone, and estradiol were determined. During the first hour, cortisol levels decreased significantly in both groups and reached a plateau during the second hour, which period was considered to represent resting levels of the hormones. The amenorrhea group showed higher mean (+/- SE) resting levels of immunoreactive beta-endorphin (11.0 +/- 0.8 versus 8.3 +/- 0.6 pg/ml, p less than 0.05) and cortisol (274 +/- 35 versus 134 +/- 14 nmol/L, p less than 0.001) and lower mean resting levels of prolactin (2.4 +/- 0.3 versus 5.7 +/- 1.1 ng/ml, p less than 0.01), luteinizing hormone (4.0 +/- 0.7 versus 10.5 +/- 1.8 IU/L, p less than 0.01), and estradiol (0.09 +/- 0.01 versus 0.19 +/- 0.07 nmol/L, p less than 0.05) than the control group. These results suggest that exercise increases basal endorphin secretion in amenorrheic women and support the theory that increased opioid activity may be involved in the pathophysiology of exercise-associated amenorrhea.
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PMID:Plasma immunoreactive beta-endorphin in exercise-associated amenorrhea. 293 46

The plasma beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) response to acute exercise and the relationship of these opioid peptides to basal and luteinizing hormone-releasing hormone (LRH)-stimulated luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion was studied in eight normal male volunteers. Acute exercise resulted in a rise in plasma beta-LPH levels that returned to base line when measured 60 min after exercise. Plasma beta-EP levels did not demonstrate any rise when measured immediately after 20 min of exercise or at 60 min after exercise. Serum LH concentrations in individual volunteers declined to nadir values 60-180 min after exercise after which they showed a rebound to levels higher than the preexercise values in three of five volunteers in whom nadir LH levels were attained before the final (180 min) measurement. Serum FSH concentrations were unaltered by exercise. Acute exercise similarly did not alter the LH/FSH response to exogenous LRH stimulation. Pretreatment of the volunteers with the narcotic antagonist, naloxone, failed to alter the postexercise or LRH-stimulated LH and FSH release. The data suggest that beta-EP does not exert a suppressive effect on LH secretion after acute exercise in normal human males. Whether the suppression of LH secretion after acute exercise in unconditioned males is due to factor(s) cosecreted with beta-LPH, an increase in brain beta-EP or to alternate mechanisms such as alteration in central dopaminergic or GABAergic tone remains to be established.
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PMID:Beta-endorphin/beta-lipotropin release and gonadotropin secretion after acute exercise in normal males. 294 41

In freely moving rats, ovine corticotropin-releasing factor (CRF) and rat CRF, which are equipotent in stimulating adrenocorticotropin (ACTH) release, can exert this effect after either i.v. or intracerebroventricular (i.c.v.) administration. Oxytocin and epinephrine also elevate plasma ACTH levels, an effect that is abolished by immunoneutralization of endogenous CRF. Inasmuch as oxytocin and epinephrine show additivity with CRF, these results suggest that these two secretagogues stimulate ACTH secretion in vivo by interacting with endogenous CRF. Apart from its effect on ACTH release, CRF injected i.c.v. markedly inhibits luteinizing hormone (LH), but not follicle-stimulating hormone, secretion in rats in the absence of circulating levels of steroids. A similar effect is observed after i.c.v. administration of sauvagine, a peptide analogous to CRF, whereas arginine vasopressin exhibits lower potency and shorter duration of action than CRF. Because these peptides do not modify LH release by cultured pituitary cells, they probably lower plasma LH levels through centrally mediated mechanisms. These results indicate that CRF can exert a broad spectrum of action to regulate pituitary function directly or indirectly.
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PMID:Effects of corticotropin-releasing factor, neurohypophyseal peptides, and catecholamines on pituitary function. 298 40

Currently available measurements of beta-endorphin and beta-lipotropin in exercising women are in excellent agreement and indicate a 2-3 fold increase over basal levels. Possible effects of exercise upon the transfer of endorphins from the peripheral circulation to the brain are examined, and evidence is presented that suggests the occurrence of a concomitant exercise-related increase of endorphins in both humoral and central nervous system compartments. Steady-state measurements of circulating luteinizing hormone and follicle-stimulating hormone levels in oligo-amenorrheic athletes, on the other hand, do not agree. It is felt that the lack of consensus may be attributable partly to technical inadequacies and partly to lack of awareness of the need for frequent sampling. The bulk of the findings suggest a tendency for luteinizing hormone levels to be low and follicle-stimulating hormone levels to be normal or low, a pattern compatible with repeated activation of the CRH-ACTH-POMC system as a result of exercise.
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PMID:Endorphins and exercise in females: possible connection with reproductive dysfunction. 298 15

Chromogranin was demonstrated by immunohistochemistry in the cytoplasm of human beta-thyrotropin, human beta-follicle-stimulating hormone-, human beta-luteinizing hormone-, and human alpha-subunit-containing cells of the non tumorous human adenohypophyses. Some surgically removed human beta-thyrotropin-, human beta-follicle-stimulating hormone-, human beta-luteinzing hormone-, and human alpha-subunit-producing pituitary adenomas, as well as some null cell-adenomas, exhibited chromogranin immunoreactivity, whereas adenomas storing human growth hormone, human prolactin, or corticotropin were negative. Chromogranin immunopositivity was variable in extent and intensity; not every glycoprotein-producing cell could be immunostained in the nontumorous adenohypophysis and the majority of chromogranin-containing adenomas showed only focal positivity. No explanation can be offered for this variability. The demonstration of chromogranin by the avidin-biotin-peroxidase technique may be helpful in the immunohistochemical characterization of some glycoprotein hormone-producing pituitary adenomas, as well as null-cell adenomas of the human pituitary.
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PMID:Immunohistochemical localization of chromogranin in human hypophyses and pituitary adenomas. 298 72

This study was designed to compare the responsiveness of adrenocorticotropin (ACTH) and cortisol secretion to corticotropin-releasing factor (CRF) in the morning and early evening in normal human subjects. Synthetic ovine CRF (1.0 micrograms/kg) or normal saline, was administered as an i.v. bolus injection to six normal males at 900 h and 1700 h. Blood samples were obtained before and 15, 30, 60, 90 and 120 min after CRF or saline injection. Significant increases in plasma ACTH and cortisol levels were observed in all subjects at the both time of testing after CRF injection. The net increments in the areas under the concentration curve (areas in the CRF experiment minus those in the saline control experiment) were not statistically different for both ACTH (mean +/- SEM: 41.0 +/- 10.6 pg/ml h in the morning: 51.1 +/- 8.9 pg/ml h in the evening) and cortisol (mean +/- SEM: 28.5 +/- 5.0 micrograms/dl h in the morning; 36.2 +/- 4.0 micrograms/dl h in the evening). Also no significant difference was observed in net increment, peak level and the ratio of peak level to the basal level of ACTH and cortisol after CRF injection. There were no appreciable changes in plasma concentrations of growth hormone, thyroid-stimulating hormone or prolactin, although slight but statistically significant rises in plasma levels of luteinizing hormone and follicle-stimulating hormone were observed. These results suggest that there is no significant difference in responsiveness of the pituitary-adrenal axis to CRF in the morning (900 h) and early evening (1700 h), and thus the time of day will not necessarily have to be considered when CRF is used between these times in a clinical test to evaluate pituitary ACTH reserve.
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PMID:Responses of plasma adrenocorticotropin and cortisol to intravenous injection of synthetic ovine corticotropin releasing factor in the morning and early evening in normal human subjects. 300 29

Cardiac atrial muscle cells produce a polypeptide hormone that plays a role in the control of water and electrolyte balance and blood pressure. The circulating form of this hormone is the atrial natriuretic peptide (ANP), which contains 28 amino acids. Various immunohistochemical studies have shown that ANP is present in many areas of the central nervous system, including the median eminence. In our studies, we investigated the effect of ANP in a superfused rat pituitary cell system. When ANP was administered at increasing concentrations (0.01 microM to 1 microM), it caused a significant dose-related stimulation of the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). The lowest effective dose of ANP in our system was 0.03 microM. When ANP and LH-releasing hormone were administered together, the response was prolonged and had the characteristics of ANP-stimulated LH and FSH release. In contrast with some previous reports, ANP in high concentration (1 microM) consistently induced a small but significant stimulation of the release of corticotropin. ANP did not influence the basal release of prolactin, growth hormone, and thyrotropin.
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PMID:Effect of atrial natriuretic peptide on gonadotropin release in superfused rat pituitary cells. 301 Feb 98

The effect of chronic administration of adrenocorticotropin on ovarian follicular development was studied. Twelve nonlactating Holstein cows received either 100 IU adrenocorticotropin (n = 6) or saline (n = 6) at 12-h intervals, commencing d 16 and continuing until d 23 of an induced estrous cycle (estrus = d 0). Cows were slaughtered on d 24, ovaries collected, and number of visible antral follicles recorded. Estradiol-17 beta, androstenedione, and testosterone in follicular fluid, and luteinizing hormone and follicle-stimulating hormone receptors in follicular tissue of the largest follicles were determined. Largest follicles were classified as ovulatory or nonovulatory based on the estrogen to androgen ratio. One cow treated with adrenocorticotropin, but none treated with saline, had ovulated by slaughter. The numbers of small, medium, and large antral follicles were 0, 1, and 5 for cows treated with adrenocorticotropin and 0, 1, and 6 for cows treated with saline. Follicular diameter (15.0 +/- 1.0 versus 14.0 +/- 2.0 mm) and follicular fluid volume (2.9 +/- .8 versus 2.2 +/- .5 ml) of the largest follicle in cows treated with adrenocorticotropin or saline were not different. No differences were found in the number of luteinizing hormone and follicle stimulating hormone receptors nor in the proportion of ovulatory versus nonovulatory follicles between treatments. We conclude that adrenocorticotropin administered at 100 IU every 12 h during the follicular phase does not significantly alter follicular development in the nonlactating dairy cow.
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PMID:Follicular development after administration of adrenocorticotropin to nonlactating Holstein cows. 301 65


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