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 present study aimed at evaluating the effect of human beta-endorphin on pancreatic hormone levels and on glucose metabolism in normal subjects. Infusion of 143 nmol/h beta-endorphin in 7 subjects caused a significant rise in plasma glucose concentrations (+ 1.7 +/- 0.3 mmol/l) which was preceded by a significant increase in peripheral plasma glucagon levels (+ 44 +/- 13 ng/l). No changes occurred in the plasma concentrations of insulin and catecholamines (adrenaline and noradrenaline). The influence of beta-endorphin per se on glucose homeostasis was studied in 7 other subjects using the euglycaemic clamp technique in which the endocrine pancreatic function was fixed at its basal level with somatostatin together with replacement of basal insulin and glucagon by the exogenous infusion of these hormones. In this new metabolic conditions, beta-endorphin failed to have significant influences on the various parameters of tracer-estimated glucose metabolism (production, utilization, and clearance) and on the plasma levels of the gluconeogenic precursors (glycerol and alanine). Moreover, the levels of pancreatic and counterregulatory hormones (cortisol and catecholamines) were not different between beta-endorphin and control studies. We conclude that the naturally occurring opioid peptide beta-endorphin produced an hyperglycaemic effect in man which appears to be mediated by glucagon. The opioid seems to have no direct effect on glucose metabolism. These results suggest that the metabolic effects of beta-endorphin in normal man are secondary to its impact on pancreatic hormone secretion and not a consequence of a direct modulation of glucose metabolism.
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PMID:Primary role of glucagon release in the effect of beta-endorphin on glucose homeostasis in normal man. 288 94

beta-Endorphin stimulates glycerol release from adipose tissue in vitro in the rabbit. Thirty different amino acid sequences of this peptide were tested for lipolytic activity. Four turned out to be active: porcine and human beta-endorphin-(1-31), human beta-endorphin-(6-31), and human beta-endorphin-(1-5)-(16-31). Structure-activity investigations showed that for the lipolytic action of beta-endorphin the C-terminal part [longer than beta-endorphin-(27-31)] is relatively important. Of special importance seems to be the C-terminal amino acid residue, because none of the sequences lacking the last two amino acid residues was lipolytically active. Furthermore, a different lipolytic response to beta-endorphin was obtained in starved, ad libitum-fed, and starved-refed animals, showing that the regulation of the lipolytic potency is not only mediated by peptide concentrations in the medium.
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PMID:In vitro lipolytic activity of beta-endorphin and its partial sequences. 295 Dec 44

The effects of an i.v. infusion of synthetic human beta-endorphin on the hormonal, metabolic and cardiovascular responses to surgery were investigated in female patients undergoing pelvic surgery. A beta-endorphin infusion (2 micrograms/kg as a bolus at induction of anaesthesia + 10 micrograms/kg/h for the first hour of surgery) increased plasma beta-endorphin immunoreactivity to values at least 100-fold greater than those seen during surgery in a control group of patients. In spite of this massive increase the only significant findings were a transient augmentation of the expected hyperglycaemic response and increased plasma glucagon values. There were no significant changes in ACTH, GH, insulin and cortisol secretion, in blood concentrations of lactate or glycerol, or in cardiovascular variables. Complete dissociation between plasma and cerebrospinal fluid concentrations of beta-endorphin was found even when plasma values exceeded 10,000 pmol/l in the presence of anaesthesia and surgery. These results show that the increase in circulating beta-endorphin immunoreactivity associated with clinical stress states are unlikely to modulate the associated hormonal, metabolic and cardiovascular changes.
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PMID:Beta-endorphin infusion fails to modulate the hormonal and metabolic response to surgery. 295 7

Injection of insulin to fed rats diminished the concentration of fructose 2,6-bisphosphate in white adipose tissue. Incubation of epididymal fat-pads or adipocytes with insulin stimulated lactate release and sugar detritiation and also decreased fructose 2,6-bisphosphate concentration. Such a decrease was, however, not observed in fat-pads from starved or alloxan-diabetic rats. Incubation of adipocytes from fed rats with various concentrations of glucose or fructose led to a dose-dependent rise in fructose 2,6-bisphosphate which correlated with lactate output and detritiation of 3-3H-labelled sugar. In adipocytes from fed rats, palmitate stimulated the detritiation of [3-3H]glucose without affecting lactate production and fructose 2,6-bisphosphate concentration. Incubation of epididymal fat-pads from fed rats in the presence of antimycin stimulated lactate output but decreased fructose 2,6-bisphosphate concentration. Changes in lipolytic rates brought about by noradrenaline, insulin, adenosine and corticotropin in adipocytes from fed rats were not related to changes in fructose 2,6-bisphosphate or to rates of lactate output. In fed rats, the activity of 6-phosphofructo-2-kinase was not changed after treatment of adipocytes with insulin, noradrenaline or adenosine. It is suggested that the decrease in fructose 2,6-bisphosphate concentration observed after insulin treatment can be explained by the increase in sn-glycerol 3-phosphate, an inhibitor of 6-phosphofructo-2-kinase.
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PMID:Regulation of fructose 2,6-bisphosphate concentration in white adipose tissue. 298 73

Rat brain membranes were incubated in N-ethylmaleimide (NEM, 0.5-1.0 mM) in the presence and absence of various concentrations of morphine, Leuenkephalin and human beta-endorphin (beta h-EP). After sufficient washing, the binding of dihydromorphine (DHM), [D-Ala-D-Leu]-enkephalin (DADLE) and tritiated beta h-EP was 10-40% above that of membranes treated with NEM alone. There was no additive effect of morphine and Leu-enkephalin with respect to their effect on recovery of beta h-EP binding. Evaluation of beta h-EP as protecting ligand proved to be difficult since preincubation completely inhibits subsequent DHM and DADLE binding unless a more extensive washing protocol is employed. A protocol for washing beta h-EP preincubated membranes using a Tris-phosphate buffer of pH 6 containing 150 mM NaCl, 20 mM MgCl2 and 10% glycerol was used to recover enough binding potential to evaluate the effects of beta h-EP preincubation towards NEM treatment. Preincubation with beta h-EP itself at 0.1-1.0 microM did not result in any increased recovery of opiate binding, in contrast to the findings with the other two ligands.
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PMID:Beta-endorphin does not protect alkylation of opiate receptor by N-ethylmaleimide. 299 Nov 53

The effects of sufentanil, 10 and 20 micrograms kg-1 on the hormonal and metabolic responses to coronary artery surgery were compared in 20 patients. The most important finding was that the changes in circulating beta-endorphin, ACTH, cortisol, GH, glucose, lactate and glycerol concentrations during and after cardiac surgery were similar with both doses of sufentanil. Although sufentanil prevented a significant increase in plasma beta-endorphin, ACTH and cortisol values until 6 h after cardiopulmonary bypass (CPB), a significant increase in GH secretion occurred with the onset of CPB. Plasma insulin concentrations declined significantly after 30 min CPB, but recovered after 60 min CPB with the restoration of normothermia. Blood glucose values did not change during surgery before CPB, but started to rise with the onset of CPB and continued to increase significantly in the postoperative period. Changes in blood lactate and plasma glycerol concentrations primarily reflected the load of CPB and the effects of heparin, respectively. The results show that increasing the dose of sufentanil up to 20 micrograms kg-1 does not result in better suppression of the endocrine and metabolic changes associated with cardiac surgery.
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PMID:Hormonal and metabolic responses to cardiac surgery with sufentanil-oxygen anaesthesia. 303 69

Interactions among lithium, calcium, and phorbol esters in the regulation of adrenocorticotropin hormone (ACTH) release were examined in a tumor cell line (AtT-20) of the anterior pituitary. Lithium, which blocks the phosphatase that converts inositol phosphates (IPs) to inositol, increases the levels of IPs in these cells and stimulates ACTH release. This ion potentiates the ability of calcium, an activator of phospholipase C, to raise levels of IPs in these cells and to stimulate ACTH secretion. Pretreatment of AtT-20 cells with calcium specifically abolishes the ACTH release response to lithium or calcium, a result suggesting that these secretagogues may act through a common mechanism to induce hormone secretion. Prior exposure of AtT-20 cells to either lithium or calcium also attenuates the ACTH release induced by phorbol ester, an activator of protein kinase C. To examine the link among lithium, calcium, phosphatidylinositol (PI) turnover, and phorbol ester-evoked ACTH secretion, AtT-20 cells were treated with 1-oleoyl-2-acetoyl-sn-3-glycerol (OAG), an analogue of the diacylgylcerols that are formed by phospholipase C during PI metabolism and that also activate protein kinase C. OAG itself does not alter ACTH release or the levels of IPs in AtT-20 cells. Pretreatment of AtT-20 cells with OAG, however, selectively blocks the ACTH release response to lithium, calcium, or phorbol ester. Furthermore, such pretreatment reduced the ability of lithium to increase levels of IPs. The results suggest that one mechanism of action of lithium is to potentiate selectively an action of calcium, possibly the stimulation of phospholipase C activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interactions among lithium, calcium, diacylglycerides, and phorbol esters in the regulation of adrenocorticotropin hormone release from AtT-20 cells. 303 56

Chronic treatment of rats with dexfenfluramine decreased the concentrations of circulating corticosterone, fatty acid, glycerol, and triacylglycerol after feeding a test load of fructose. It also decreased the rise in adrenalin in the blood of rats that were anaesthetized with urethane. These effects of dexfenfluramine probably result from changes in the metabolism of 5-HT in the CNS and consequent alterations in hormonal balance. It is proposed that the long-term metabolic effects of dexfenfluramine could be explained by a decrease in the effectiveness of stress hormones (e.g., glucocorticoids, corticotropin, catecholamines, glucagon) in regulating metabolism since these hormones antagonize many of the actions of insulin. This hypothesis also identifies the possibility that the ability of dexfenfluramine to decrease an exaggerate stress response could alleviate some of the potential risk factors associated with atherosclerosis including obesity and maturity onset diabetes.
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PMID:Metabolic and hormonal effects of dexfenfluramine on stress situations. 318 Jan 10

Fifty peptides and hormones from the hypophysis, hypothalamus, gastrointestinal tract and from other origins were tested for lipolytic activity in the isolated rabbit fat cell. Eight peptides derived from the precursor hormone proopiocortin stimulated glycerol release while all the other peptides and hormones showed no lipolytic activity. The most potent lipolytic peptide was alpha-MSH which also had the lowest minimal effective dose, followed by beta-lipotropin, ACTH and beta-MSH. The lipolytic activity was not influenced by the use of different collagenases or the cells from different breeds of rabbits.
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PMID:Peptide hormones and lipolysis in rabbit adipocytes. 399 60

The proopiocorticomelanotropin (POMC) sequence beta-lipotropin stimulates glycerol release from incubated rabbit adipocytes at a minimal concentration of 10(-9) mol/L. However, when lipolysis inhibiting substances (eg, fatty acids and adenosine) and contaminating peptide degrading activity are continuously removed by fat cell perifusion, the sensitivity is increased to 10(-13) and partly to 10(-14) mol/L beta-lipotropin. This higher sensitivity of the perifused adipocyte could also be demonstrated with alpha-MSH (from 5 X 10(-10) to 10(-13) mol/L). The restimulation of glycerol release was shown for both peptides. We conclude that POMC peptides might be involved in the regulation of lipolysis since the minimal effective concentrations are near to plasma concentrations.
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PMID:Physiologic concentrations of beta-lipotropin stimulate lipolysis in rabbit adipocytes. 399 75


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