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 hypothalamic-pituitary function of 93 children, who had received central nervous system (CNS) prophylaxis as part of their therapy for acute lymphocytic leukemia (ALL), and who remained in continuous complete remission, was evaluated retrospectively. Treatment regimens included--Group I: 31 subjects, intrathecal methotrexate (IT MTX); Group II: 31 subjects, IT MTX plus 2400 rad cranial irradiation; and Group III: 31 subjects, IT MTX and intravenous intermediate-dose methotrexate. Serum thyroid-stimulating hormone (TSH) and T4 levels were normal. All participants had normal adrenocorticotropic hormone (ACTH) secretion as assessed by plasma cortisol responses to insulin hypoglycemia. Urinary follicle-stimulating hormone (FSH) and luteinizing hormone (LH) excretion of pubertal and postpubertal patients (N = 37) was appropriate, except for one subject from Group I who had an abnormally high output of gonadotropins, and one from Group II who had abnormally low levels. Growth hormone (GH) responses were subnormal after sequential arginine-insulin stimulation as follows--Group 1: 3 of 31 patients; Group II: 6 of 25 patients; and Group III: 2 of 29 patients. Nevertheless, all children had normal linear growth. It was concluded that the three forms of CNS prophylaxis evaluated had no long-term adverse effect on TSH and ACTH secretion. FSH-LH production appears to be normal, but final judgment must await follow-up studies because 60% of the patients were prepuberteral or still receiving chemotherapy. Eleven patients had subnormal GH responses after pharmacologic stimulation of the pituitary, but long-term linear growth was unaffected.
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PMID:Hypothalamic-pituitary function of children with acute lymphocytic leukemia after three forms of central nervous system prophylaxis. A retrospective study. 375 92

Pituitary cells were isolated from adult human pituitary glands obtained at autopsy 4-12 h postmortem by enzyme treatment (collagenase and dispase) and by Percoll density gradients. Cells thus isolated were maintained in culture for more than 6 months. By immunoperoxidase staining methods using rabbit sera monospecific against various pituitary hormones, a large number of cultured cells reacted positively. The hormones identified in these cells were growth hormone, prolactin, adrenocorticotropin, follicle-stimulating hormone, luteinizing hormone and thyrotropin. Electron-microscopic examination of cultured cells revealed the presence of secretory granules in cytoplasm characteristic of in vivo human pituitary cells.
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PMID:Isolation, culture and cell-type identification of adult human pituitary cells. 408 22

Antibodies directed against human follicle-stimulating hormone (FSH) were demonstrated in rabbit serum by neutralization of biological activity. Antibodies that bound FSH-(131)I were produced in rabbits and guinea pigs by repeated injections of FSH. By (131)I immunochemical methods, we found that at least 90% of the FSH-(131)I-binding antibody failed to distinguish the four human glycoprotein hormones: FSH, luteinizing hormone, chorionic gonadotropin, and thyrotropin, purified as well as endogenous hormone in plasma. Neither growth hormone, adrenocorticotropin, nor a variety of glycoproteins or animal plasmas were able to react with these antibodies.
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PMID:Antibody to human follicle-stimulating hormone: cross-reactivity with three other hormones. 429 78

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

The endogenous opiate system is involved in the regulation of numerous bodily functions, but the literature suggests that the effects of endogenous opioids differ among species and between animals and man. Naltrexone, a relatively pure opiate antagonist, appears to have significant effects on the secretion of the gonadotropins (luteinizing hormone and follicle-stimulating hormone), adrenocorticotropin (ACTH), cortisol, and probably catecholamines. Naltrexone appears to have minor or no effects on prolactin, the pituitary-thyroid axis, growth hormone, insulin, glucagon, vasopressin, and the gut hormones. Naltrexone also seems to reduce food intake and cause weight loss in humans. The dosages of opiate antagonist and the presence of other variables play a major role in the responses seen in various studies.
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PMID:Endocrine and metabolic effects of opiate antagonists. 608 67

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.
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PMID:Elevated plasma levels of beta-endorphin in a group of women with polycystic ovarian disease. 609 52

In a significant proportion of patients with acromegaly, a non-specific increase in plasma growth hormone (GH) has been recognized following administration of thyrotropin-releasing hormone (TRH) or luteinizing hormone-releasing hormone (LH-RH), probably due to the lack of the specificity of the receptor in their tumor cells. In this study, the effects of corticotropin-releasing factor (CRF), a newly isolated hypothalamic hormone, in addition to TRH and LH-RH, on plasma levels of GH and the other anterior pituitary hormones were evaluated in 6 patients with acromegaly. Synthetic ovine CRF (1.0 microgram/kg), TRH (500 micrograms) or LH-RH (100 micrograms) was given as an iv bolus injection, in the morning after an overnight fast. Blood specimens were taken before and after injection at intervals up to 120 min, and plasma GH, adrenocorticotropin (ACTH), thyrotropin, prolactin, luteinizing hormone, follicle-stimulating hormone and cortisol were assayed by radioimmunoassays. A non-specific rise in plasma GH was demonstrated following injection of TRH and LH-RH, in 5 of 6 and 2 of 5 patients, respectively. In all subjects, rapid rises were observed in both plasma ACTH (34.3 +/- 6.2 pg/ml at 0 min to 79.5 +/- 9.5 pg/ml at 30 min, mean +/- SEM) and cortisol level (9.1 +/- 1.3 micrograms/dl at 0 min to 23.4 +/- 1.2 micrograms/dl at 90 min). However, plasma levels of GH and the other anterior pituitary hormones did not change significantly after CRF injection. These results indicate that CRF specifically stimulates ACTH secretion and any non-specific response of GH to CRF appears to be an infrequent phenomenon in this disorder.
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PMID:Effect of synthetic ovine corticotropin-releasing factor on growth hormone secretion in patients with acromegaly. 609 67

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

The effects of mazindol, an anorexiant, on the secretion of anterior pituitary and adrenocortical hormones were examined in healthy male volunteers and in patients with Addison's disease. In healthy male volunteers, significant elevations in plasma ACTH, beta-endorphin, beta-lipotropin and growth hormone were induced by mazindol administration, though no changes were observed in plasma thyrotropin, luteinizing hormone, follicle-stimulating hormone or prolactin. Plasma ACTH increased in patients with Addison's disease, too. In addition, plasma cortisol increased, without a change in the plasma aldosterone levels after mazindol administration to normal subjects.
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PMID:Acute effects of mazindol on the secretion of ACTH, beta-lipotropin, beta-endorphin and cortisol in man. 609 40

The Swarm chondrosarcoma is a hormone-responsive tumor whose growth is dependent on growth hormone, somatomedins, and glucocorticoids. Our previous work showed that partial functional hypophysectomy can be achieved by chronic administration of the luteinizing hormone-releasing hormone (LH-RH) analog [D-Trp(6)]LH-RH, which lowers blood levels of LH and follicle-stimulating hormone. We have also demonstrated that somatostatin (SS)-28 or analogs of SS-14 depress serum prolactin, growth hormone, and corticotropin (ACTH) levels. Consequently, we investigated the effect of subcutaneous injection of these analogs on the growth of Swarm chondrosarcoma 3 days after transplanting it into male Sprague-Dawley rats. At autopsy, tumor volume was measured and tumors and various organs were weighed. In rats treated with three different analogs of SS-14, [p-NH(2)-Phe(4)]SS, [D-5-F-Trp(8)]SS, and [D-5-MeO-Trp(8)]SS, in doses of 30 mug once or twice daily for 14-30 days, there was a significant reduction in tumor volume and/or weight as compared with control rats. The longer acting SS-28 or its analog Val-Gly-Tyr-Val-Ile-Leu-Gly-SS-28, given in doses of 30 mug/day for 22-30 days, also significantly decreased tumor weight and/or volume. In three experiments, [D-Trp(6)]LH-RH (30-60 mug/day), administered alone or together with analogs of SS-14, decreased tumor weight and/or volume. Serum growth hormone and prolactin levels in rats bearing the tumors were significantly decreased after treatment with [D-5-F-Trp(8)]SS or with [D-Trp(6)]LH-RH. The inhibition of growth of the Swarm chondrosarcoma in rats by these analogs suggests that they might lead to a new endocrine therapy for chondrosarcomas, osteosarcomas, and related hormone-dependent neoplasias.
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PMID:Inhibition of growth of the transplantable rat chondrosarcoma by analogs of hypothalamic hormones. 613 78


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