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)

A radioimmunoassay method for beta-melanocyte-stimulating hormone (beta-MSH) has been developed and utilized in the identification and quantification of this hormone in human plasma and tissues. The concentration of beta-MSH in two human pituitary glands was found to be approximately 350 mug/g. beta-MSH was identified in the tumor tissue of all 11 patients with the ectopic ACTH syndrome who were studied; concentrations in individual cases ranged from 3 to 1600 ng/g. In plasma of chronically hyperpigmented patients with Addison's disease, Cushing's disease (after bilateral adrenalectomy), and the ectopic ACTH syndrome, beta-MSH concentrations of 0.5-6 ng/ml were found. The degree of clinical hyperpigmentation was well correlated with the quantity of beta-MSH in the plasma. beta-MSH concentrations in the plasma of normal subjects were less than 0.09 ng/ml. In all of these circumstances, bioassays for MSH were also performed, and it was found that most of the biologic MSH activity of the plasma and tissues could be accounted for by beta-MSH.
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PMID:Radioimmunoassay of beta-MSH in human plasma and tissues. 429 52

The regulation of plasma beta-melanocyte-stimulating hormone (beta-MSH) in man has been studied utilizing a radioimmunoassay previously described (1). In normal subjects plasma beta-MSH values ranged from 20 to 110 pg/ml. Metyrapone increased and dexamethasone decreased plasma beta-MSH levels. Surgical stress stimulated beta-MSH secretion. Plasma beta-MSH levels were elevated in patients with untreated Addison's disease and untreated congenital adrenal hyperplasia, and these levels fell to normal during glucocorticoid therapy. In patients with Cushing's syndrome due to pituitary adrenocorticotropic hormone (ACTH) excess, plasma beta-MSH was slightly elevated before treatment. In those patients who developed pituitary tumors and hyperpigmentation after bilateral adrenalectomy, plasma beta-MSH was greatly elevated. In patients with Cushing's syndrome due to adrenal tumor, plasma beta-MSH was subnormal. In patients with the ectopic ACTH syndrome, the levels of plasma beta-MSH were high. Plasma beta-MSH had a diurnal variation in normal subjects, patients with Addison's disease, and patients with congenital adrenal hyperplasia; but the normal diurnal variation was lost in patients with Cushing's disease. In patients with high plasma beta-MSH, simultaneous determinations of plasma ACTH showed close correlation between the degree of elevation of ACTH and that of beta-MSH. In extracts of tumors from patients with the ectopic ACTH-MSH syndrome the quantities of the two hormones were roughly equivalent. In patients with hyperpigmentation due to a variety of disorders other than pituitary-adrenal abnormalities, plasma beta-MSH was normal. It is concluded that the secretion of beta-MSH is regulated by the same factors that regulate ACTH.
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PMID:Normal and abnormal regulation of beta-msh in man. 430 2

The circadian rhythm, suppression with dexamethasone, and stimulation by corticotropin-releasing hormone (CRH) of plasma immunoreactive (IR) proopiomelanocortin N-terminal (NT) and IR-ACTH were studied in nine normal subjects and two patients with Addison's disease. The RIA for human NT (hNT) used was specific for NT except for partial cross-reactivity with gamma 2MSH. In normal subjects, plasma IR-hNT and IR-ACTH had almost parallel circadian rhythms and were suppressed by dexamethasone. The mean plasma levels of IR-hNT and IR-ACTH at 0800 h were 140 +/- 23 (SD) and 23 +/- 5 pg/ml, respectively. Plasma IR-hNT increased in parallel with IR-ACTH 15 to 30 min after iv injection of 100 micrograms ovine CRH. Maximum percent increases in plasma IR-hNT and IR-ACTH were 185 +/- 47 and 235 +/- 10%, respectively. In Addison's disease, on the other hand, plasma levels of IR-hNT and IR-ACTH were markedly elevated and the circadian rhythms were parallel. The mean plasma IR-hNT and IR-ACTH levels at 0900 h were 4363 and 1750 pg/ml, respectively. These results suggest that plasma hNT and ACTH are produced from a common precursor in the pituitary gland and secreted concomitantly under various physiological conditions such as stimulation by CRH and inhibition by glucocorticoid.
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PMID:Human plasma proopiomelanocortin N-terminal peptide and adrenocorticotropin: circadian rhythm, dexamethasone suppression, and corticotropin-releasing hormone stimulation. 608

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

A method is described for the simultaneous assay of non-conjugated androstenedione, dehydroepiandrosterone, testosterone, cortisol, aldosterone and 18-hydroxycorticosterone in urine. The method involves solid-phase extraction, automatic high performance liquid chromatography and subsequent radioimmunological quantitation of the individual steroids. Excretion rates of these urinary free steroids were determined in normal males and females. There were no significant sex differences in excretion rates, although both urinary free testosterone and dehydroepiandrosterone were distinctly lower in females than in males. Representative measurements of the excretion rates of patients with Cushing's disease, Addison's disease, ectopic corticotropin syndrome and hirsutism were made. The present method has been shown to be well suited for routine purposes. Its final diagnostic significance for monitoring alterations in glucocorticoid, mineralocorticoid and androgenic activity of the adrenal cortex has yet to be explored.
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PMID:Estimation of urinary unconjugated androstenedione, dehydroepiandrosterone, testosterone, cortisol, aldosterone and 18-hydroxycorticosterone as a potential tool for assessing adrenal status. 622 40

Using a specific radioimmunoassay for gamma-melanotropin (gamma-MSH), one of the predicted fragments in the amino-terminal portion of the adrenocorticotropin(ACTH)-beta-lipotropin (beta-LPH) precursor, gamma-MSH-like immunoreactivity (gamma-MSH-LI) was detected in human plasma from 4 of 5 patients with Addison's disease and 2 of 3 patients with Nelson's syndrome. None of the normal subjects or patients with Cushing's disease showed detectable concentrations (more than 150 pg/ml) of gamma-MSH-LI. gamma-MSH-LI was secreted concomitantly with ACTH-like immunoreactivity (ACTH-LI) and beta-endorphin-like immunoreactivity (beta-endorphin-LI) in response to insulin-induced hypoglycemia and the administration of lysine-vasopressin. Conversely, intravenous injection of cortisol lowered plasma concentrations of gamma-MSH-LI concomitantly with those of ACTH-LI and beta-endorphin-LI. Gel chromatographic studies of the plasma extracts showed a single peak of gamma-MSH-LI near the elution position of human beta-LPH. These results suggest that gamma-MSH-LI in human plasma is present as a big form and that this big gamma-MSH is secreted concomitantly with ACTH and beta-endorphin.
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PMID:Concomitant secretion of Y-MSH with ACTH and beta-endorphin in humans. 625 36

We have studied the relative concentrations of the human immunoreactive (IR) peptides gamma-lipotropin (hgammaLPH, [1-58]hbetaLPH), beta-lipotropin (hbetaLPH), and beta-endorphin (hbetaEND, [61-91]hbetaLPH) using gel exclusion chromatography together with a specific radio-immunoassay (RIA) for hgammaLPH and a RIA that (because hbetaEND is the COOH-terminus of the hbetaLPH molecule) measures both hbetaEND and hbetaLPH on an equimolar basis. In normal subjects, basal plasma IR-hgammaLPH was often undetectable (<12.5 fmol/ml), but ranged up to 21 fmol/ml, and IR-hbetaEND/hbetaLPH was 10.8+/-0.7 fmol/ml; previous studies by others suggest that most of the IR-hbetaEND/hbetaLPH was probably hbetaLPH. Both IR-hgammaLPH and IR-hbetaEND/hbetaLPH were significantly elevated (P < 0.001) in patients undergoing chronic hemodialysis (101.5+/-12.7 and 23.8+/-2.0 fmol/ml, respectively). Their IR-hgammaLPH coeluted with standard hgammaLPH as a single peak, and IR-hbetaEND/hbetaLPH coeluted with hbetaLPH; no distinct peak of IR-hbetaEND was observed. In patients with ACTH/LPH hypersecretion due to Addison's disease, Nelson's syndrome, or ectopic ACTH syndrome, IR-hgammaLPH and IR-hbetaEND/hbetaLPH were both elevated, and IR-hbetaEND/hbetaLPH eluted as two peaks, one coeluting with hbetaLPH and the other with hbetaEND. The molar concentrations of all three peptides were significantly correlated with one another. The lower concentrations of endogenous IR-hbetaEND observed may be due in part to its apparent shorter plasma half-life, as estimated in an Addison's patient given a cortisol infusion. The biologic significance of these three peptides in circulating blood is still unknown. The increased levels of hbetaLPH and hgammaLPH in plasma of patients with chronic renal failure suggest that the kidney may be an important organ for their metabolism.
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PMID:Simultaneous assay of immunoreactive beta-lipotropin, gamma-lipotropin, and beta-endorphin in plasma of normal human subjects, patients with ACTH/lipotropin hypersecretory syndromes, and patients undergoing chronic hemodialysis. 625 10

Thirteen patients with either Addison's disease, or Cushing's disease treated by bilateral adrenalectomy, were infused with the long-acting met-enkephalin analogue DAMME. In patients with Addison's disease significant and pronounced falls in ACTH and N- and C-terminal beta-LPH were seen; chromatography suggested that beta-endorphin fell concomitantly. Three out of four patients with Cushing's disease who had not received pituitary irradiation, also showed a decrease in plasma ACTH and N- and C-terminal beta-LPH; however, no change was seen in any of the irradiated patients. The changes were naloxone reversible. The levels of plasma met-enkephalin were normal and did not change after DAMME in any group of patients. These results are interpreted as suggesting that there are inhibitory opiate receptors controlling the release of ACTH, beta-LPH, and beta-endorphin.
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PMID:The effects of a met-enkephalin analogue on ACTH, beta-LPH, beta-endorphin and MET-enkephalin in patients with adrenocortical disease. 627 21

1. The blood pressure, renal and metabolic effects of adrenocorticotropic hormone (ACTH) have been studied in six normotensive subjects and two patients with Addison's disease on maintenance steroid therapy. 2. In normotensive subjects, 5 days ACTH treatment (0.5 mg 12 hourly) was associated with a rise in systolic blood pressure and mean arterial pressure. There was a small rise in diastolic pressure but no consistent change in heart rate. Plasma sodium increased and plasma potassium fell. Serum creatinine and urea concentrations were unchanged. Fluid intake increased and urine output was unchanged but ACTH withdrawal was associated with a diuresis. There was an initial reduction in urinary sodium excretion and a natriuresis after ACTH withdrawal. Plasma volume and body weight rose. 3. ACTH produced increases in plasma cortisol, 11-deoxycortisol, corticosterone, deoxycorticosterone, aldosterone, 17 alpha-hydroxyprogesterone and 17 alpha,20 alpha-dihydroxyprogesterone. Plasma renin concentration fell. 4. Patients with Addison's disease showed no change in blood pressure or in any other metabolic variable studied. 5. The effects of ACTH in man resembled those found in sheep.
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PMID:Blood pressure, renal and metabolic effects of ACTH in normotensive man. 627 70

Human ACTH-producing tumor and plasma have been examined by gel filtration and ion exchange chromatography to detect the possible presence of reported multiple forms of immunoreactive beta-endorphin (I-EP) Ion exchange chromatography of I-EP obtained from gel filtration showed four components of I-EP [two major peaks in the positions of EP-(1-31) and EP-(1-27) and two minor peaks in the positions of N-acetyl EP-(1-31) and N-acetyl EP-(1-27)] in two ectopic ACTH-producing lung cancers, and two components of I-EP [the major peak in the position of EP-(1-31) and minor peak in the position of N-acetyl EP-(1-31) in an ectopic ACTH-producing thyroid cancer. Only a single peak in the position of EP-(1-31) was present in plasma from a patient with Nelson's sindrome and a patient with Addison's disease, in the pituitary adenomas from six patients with Cushing's disease, and in the nontumorous pituitary tissues from a patient with Cushing's disease and a patient with acromegaly. These data suggest that the posttranslational processing of EP in human pituitary is different from that in the ectopic ACTH-producing tumor.
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PMID:Multiple forms of immunoreactive beta-endorphin are present in an ectopic adrenocorticotropin-producing tumor but not in normal pituitary or pituitary adenomas. 627 95


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