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)

In 72 patients with end-stage renal failure and 70 healthy subjects, the influence of blockade of opioid receptors by naloxone on secretion of prolactin, lutropin (LH), follitropin (FSH), adrenocorticotropin (ACTH), somatotropin (HGH), insulin (IRI), glucagon (IR-G), parathyroid hormone (PTH) and calcitonin (CT) was studied. Administration of naloxone stimulated luliberin-induced LH and FSH secretion quantitatively equally in patients and controls. Blockade of opioid receptors was followed by a less marked suppression of chlorpromazine-induced prolactin secretion but by a higher response of hypoglycemia-induced ACTH secretion in uremic patients than in controls. In addition, a less marked suppressive effect of naloxone was noted on hypoglycemia-induced HGH secretion in chronic renal failure as compared with controls. Blockade of opioid receptors improved significantly glucose tolerance and glucose-induced insulin secretion in uremic patients and suppressed nearly completely glucagon secretion response during the second phase of a glucose tolerance test. Finally, administration of naloxone was followed by a blunted response of Ca-induced CT secretion and suppression of PTH. Data presented in this paper suggest the existence of hyperendorphinism in end-stage renal failure.
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PMID:Effects of naloxone administration on endocrine abnormalities in chronic renal failure. 303 7

Plasma epinephrine (EPI), norepinephrine (NE), beta-endorphin, and corticotropin (ACTH) responses were measured during insulin-induced hypoglycemia in normal subjects and in patients with either multiple system atrophy (MSA) or idiopathic orthostatic hypotension (IOH). In normal subjects, there was a striking rise in EPI, NE, beta-endorphin, and ACTH following the nadir of hypoglycemia. Both beta-endorphin and ACTH responses were significantly lower than normal in patients with MSA, in contrast to normal levels in IOH patients. No correlation was observed between the degree of adrenergic insufficiency and the beta-endorphin and ACTH responses. The normal peptide responses in IOH are consistent with involvement limited to the peripheral sympathetic nervous system, whereas lesions in the central nervous system in MSA interfere with release of beta-endorphin and ACTH in response to hypoglycemia. The strong correlation between beta-endorphin and ACTH levels is consistent with their common origin. Peripheral adrenergic activity is not essential for beta-endorphin and ACTH release in humans.
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PMID:Beta-endorphin, ACTH, and catecholamine responses in chronic autonomic failure. 303 91

Peripheral venous plasma free and sulfoconjugated catecholamines, dopamine (DA), noradrenaline (NA) and adrenaline (A) were measured in normal men (n = 6-7) during conditions significantly altering adrenal and sympathoadrenal function (influence of corticotropin, furosemide, hypoglycaemia and clonidine), after dopamine receptor blockade with metoclopramide and after meals. Median (range) basal plasma free DA concentration was 0.13 (0-0.72) nmol/l and median (range) basal plasma conjugated DA concentration was 15.16 (6.34-45.03) nmol/l. Meals increased plasma sulfoconjugated DA markedly from a median value of 14.97 nmol/l during fasting experiments to a median value of 33.01 nmol/l (p less than 0.05). Plasma free DA did not change in the meal experiments. No changes in plasma DA were observed after administration of corticotropin, furosemide, clonidine, and metoclopramide or during hypoglycaemia. The results suggest that plasma sulfoconjugated DA is derived at least in part from the gastrointestinal tract and not from the sympathoadrenomedullary system as hitherto proposed.
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PMID:Plasma free and sulfoconjugated dopamine in man: relationship to sympathetic activity, adrenal function and meals. 316 58

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

The effect of type I and II diabetes in pregnancy on the circadian rhythm and diurnal excursion of plasma cortisol was studied in the second and third trimesters and post partum. Cosignor analysis demonstrated persistence during gestation of the significant circadian rhythm of the nonpregnant state. As previously reported in control pregnancies, plasma cortisol levels (24-hour mean, nadir, peak, and nadir-peak excursion) increased during gestation while the relative excursion of cortisol (expressed as the percent deviation from the 24-hour mean) was blunted. No significant difference was found between diabetic groups or when diabetic groups were compared with control subjects. Nocturnal hypoglycemia was common among diabetic women during pregnancy and post partum. Although these episodes were usually asymptomatic, the mean concomitant cortisol levels were increased over the corresponding cortisol levels of nonhypoglycemic diabetic and control subjects. We conclude that differences between control and type I and II diabetic subjects in carbohydrate tolerance or glycemic excursion are not explained by differences in cortisol levels or rhythm. The pregnancy-associated blunting of the excursion of cortisol is consistent with an autonomous source of adrenocorticotropin. Asymptomatic nocturnal hypoglycemia is common in insulin-requiring diabetic women and is associated with increased cortisol secretion.
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PMID:Circadian rhythm and diurnal excursion of plasma cortisol in diabetic pregnant women. 378 30

The effects of the long acting met-enkephalin analogue D-Ala2-MePhe4-met-enkephalin-O-ol (DAMME) and the opiate antagonist naloxone on the plasma catecholamine responses to insulin-induced hypoglycaemia have been investigated in two separate studies. DAMME depressed basal noradrenaline and adrenaline at 15 min, and blunted both the noradrenaline and adrenaline responses to hypoglycaemia. Naloxone did not alter basal plasma catecholamines, but caused a significant enhancement of the adrenaline response to hypoglycaemia. Neither DAMME nor naloxone altered the blood glucose response to insulin-induced hypoglycaemia. These data are consistent with an inhibitory modulation of endogenous opioids in the sympathoadrenal response to insulin-induced hypoglycaemia in man.
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PMID:Evidence for the participation of endogenous opioids in the sympathoadrenal response to hypoglycaemia in man. 388 88

A single intravenous injection of four hypothalamic releasing hormones-corticotropin-, growth hormone-, gonadotropin- and thyrotropin-releasing hormones-was administered to normal subjects. Except for the plasma adrenocorticotropic hormone (ACTH) level, a statistically significant increase in all anterior pituitary hormone levels occurred. Transient flushing was the only consistent side effect. In the same persons, results were compared with those obtained with insulin-induced hypoglycemia and a single-dose overnight metyrapone test. Growth hormone and cortisol responses to insulin-induced hypoglycemia were similar but prolactin increment was less than that obtained by the peptide injection. ACTH increments from both tests were substantially less than those obtained by the overnight metyrapone test. We conclude that pituitary function can be effectively studied in normal subjects by the combination of a metyrapone test with a triple bolus of growth hormone-, thytropin- and gonadotropin-releasing hormones, but not by a quadruple bolus of the hypothalamic peptides. Compared with insulin-induced hypoglycemia, this approach yields more information with fewer side effects.
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PMID:Quadruple injection of hypothalamic peptides to evaluate pituitary function in normal subjects. 391 7

Techniques are described in detail for a radioimmunoassay of plasma adrenocorticotropin (ACTH) that is capable of detecting hormone in unextracted normal human plasma at 1:5 dilution under the conditions described. The sensitivity of the assay is at the level of 1 mumug/ml (equivalent to 0.014 mU/100 ml). In normal subjects ACTH concentrations averaged 22 mumug/ml (equivalent to 0.308 mU/100 ml) plasma at 8-10 a.m. In a smaller group the concentrations averaged 9.6 mumug/ml (equivalent to 0.134 mU/100 ml) at 10-11 p.m. Although a circadian rhythm in normal subjects was not always well marked throughout the daytime hours, plasma ACTH usually fell to its lowest value in the late evening. In hospital patients who were not acutely ill, concentrations were infrequently above 100 mumug/ml in the morning and usually fell to significantly lower levels in the late evening. Severely ill hospital patients occasionally exhibited a.m. concentrations above 200 mumug/ml. In a group of subjects showing frequent spiking of plasma 17-OHCS concentrations throughout the day parallel spiking of plasma ACTH as well was generally observed.Metyrapone produced marked increases in plasma ACTH within 24 hr in all cases and generally within 3-6 hr except when started late in the day. Dexamethasone brought about a persistent reduction in plasma ACTH in a patient under continued treatment with metyrapone.Hypoglycemia, electroshock, surgery under general anesthesia, histalog and vasopressin administration were usually followed by significant increases in plasma ACTH concentration. Prior administration of dexamethasone blocked the response to hypoglycemia. Marked elevations in plasma ACTH were observed in patients with adrenal insufficiency off steroid therapy, in Cushing's disease after adrenalectomy even in the presence of persistent hypercortisolemia, and in some untreated patients with Cushing's disease. Umbilical cord blood contained higher plasma ACTH concentrations than maternal blood at delivery in seven of eight cases. After suppression of ACTH secretion by dexamethasone or cortisol. ACTH disappeared from plasma with half-times ranging from 22 min to 30 min in three cases studied.
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PMID:Radioimmunoassay of ACTH in plasma. 430 80

A radioimmunoassay for immunoreactive gamma-MSH (IR-gamma-MSH) in human plasma has been developed. The assay is capable of detecting normal basal circulating levels which range from less than 20-100 ng/1 at 0900 h. Plasma levels are raised concomitantly with ACTH during insulin induced hypoglycaemia and CRF stimulation and suppressed with dexamethasone. Chromatographic characterisation of IR-gamma-MSH in plasma demonstrates a major peak of IR-gamma-MSH, corresponding to purified glycosylated N-terminal pro-opiomelanocortin 1-76, when IR-gamma-MSH is secreted from the pituitary. In contrast IR-gamma-MSH produced ectopically appears to be heterogeneous.
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PMID:Measurement of immunoreactive gamma-MSH in human plasma. 608 29

The effect of insulin-induced hypoglycemic stress on the concentrations of immunoreactive beta-endorphin (ir beta-EP) in plasma and cerebrospinal fluid (CSF) was examined in conscious non-pregnant ewes in which the cisterna magna and a jugular vein had been previously catheterized. In control experiments, no significant changes were observed in plasma cortisol or ir beta-EP and CSF ir beta-EP concentrations. During hypoglycemia induced by intravenous injection of 20 units of insulin, plasma cortisol concentrations rose significantly, reaching a peak 1.5 h after injection. The changes in plasma ir beta-EP concentration were significantly different between hypoglycemic and normoglycemic sheep (analysis of variance, P = 0.0089). Following insulin injection, mean plasma ir beta-EP rose by 100% within 0.75 h, continued to rise six-fold over initial concentrations by 2.25 h, and remained elevated for 3.75 h. The CSF ir beta-EP concentrations following insulin injection were not significantly different from those observed in controls. These results suggest that if beta-endorphin mediated hypoglycemic stress-induced analgesia, its actions may be peripheral, not central.
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PMID:Effect of hypoglycemic stress on plasma and cerebrospinal fluid immunoreactive beta-endorphin in conscious sheep. 609


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