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 aim of this paper was to study the effect of a single dose of 14, 30 or 90 days' administration of sulpiride (SUL) (50 or 100 mg/kg), metoclopramide (MET) (20 or 40 mg/kg) or haloperidol (HAL) (2 mg/kg) on the level of leu- and met-enkephalin (ENK) in the striatum. A dose and time dependent increase of the striatal ENK level was observed after chronic administration of atypical neuroleptics SUL or MET as well as after chronic treatment with a classical cataleptogenic neuroleptic HAL. The effect of chronic administration of HAL on the striatal level of leu-enkephalin was stronger than after SUL but lower than after MET treatment. It is concluded that: 1) Chronic administration of atypical neuroleptics results in the increased level of striatal ENK similar to that after chronic treatment with classical cataleptogenic neuroleptics; 2) Apparently both more or less selective antagonists of dopaminergic D2 receptors activate the enkephalinergic system in the striatum.
Pol J Pharmacol
PMID:Chronic treatment with atypical neuroleptics sulpiride and metoclopramide increases striatal enkephalins in rat brain. 801 72

The concentrations of beta-endorphin, ACTH, insulin (IRI), glucagon (IRG), cortisol and growth hormone were determined by radioimmunoassay during oral glucose tolerance test (OGTT) performed in 13 obese patients with normal glucose tolerance and without arterial hypertension. The test was performed in random, before and after intravenous administration of 0.8 mg of naloxone. Six persons with normal body weight served as controls. Higher basal concentrations of beta-endorphin and significant increase in beta-endorphin levels during OGTT, without concomitant increase in ACTH concentrations, have been found in obese patients. No effect of naloxone on beta-endorphin liberation during OGTT was observed, though the drug caused lowering in maximal increment of beta-endorphin and paradoxically lowered the concentrations of ACTH and cortisol. The basal concentrations of beta-endorphin did not correlate with the concentrations of insulin, ACTH, cortisol and growth hormone. Elevated concentrations of insulin, lowered concentration of growth hormone and normal levels of glucose and glucagon were observed in basal conditions, and excessive responses of insulin, glucose and glucagon were observed in obese patients during OGTT. Naloxone lowered insulin response and inhibited the fall of growth hormone during OGTT but did not influence the concentrations of glucose and glucagon. No correlation was found during OGTT after naloxone between insulin and beta-endorphin, ACTH or cortisol, whereas negative correlation was observed between insulin and growth hormone. The obtained results suggest that the elevated concentrations of beta-endorphin in simple obesity may be of both hypophyseal and peripheral origin. Hyper-beta-endorphinemia observed in obesity is probably not directly responsible for hyperinsulinemia, it may, however, be responsible for lower sensitivity of tissues to the action of insulin.
Endokrynol Pol 1993
PMID:[Effect of naloxone on beta-endorphin and insulin concentrations during glucose tolerance testing in patients with simple obesity]. 805 20

The basal and hyperglycaemia-stimulated secretion of glucose, IRI and beta-endorphin (BE) were studied in subjects who had gone surgical treatment for obesity few years ago and the results were compared with those of obese subjects and lean controls. 58 persons were divided into the following groups: A-obese subjects BMI > 30, B--obese subjects 25 < BMI < 30, C--subjects treated by truncal vagotomy and gastric banding, D--subjects treated by jejunoileostomy, E--control group BMI < 25. Oral glucose (75 g) tolerance test was performed in all subjects. Blood concentration of glucose, and serum concentration of IRI and BE were studied before and 30, 60, 90 and 120 minutes after ingestion of glucose. The basal levels and areas over basal values (AOBV) of investigated parameters were evaluated. Both the basal and glucose stimulated levels of IRI and BE were higher in the obese subjects than in the control group. Truncal vagotomy and gastric banding or jejunoileostomy resulted in reduction of IRI secretion without any decrease in BE levels. The alteration of the opioid system may play some role in the pathogenesis of obesity.
Pol Arch Med Wewn 1993 Jul
PMID:[Level of beta endorphins and insulin in blood of obese subjects. Effect of surgical treatment for obesity on higher exchange parameters]. 823 1

In patients with chronic renal failure (CRF) an elevated serum beta-endorphin (BE) level and lack of a twenty-four-hour BE-secretory pattern were found. BE and other opioid peptides participate significantly in the development of the uremic syndrome and its complications. On the other hand hemodialytic treatment is an important factor influencing the concentration of most hormones. In healthy subjects insulin-induced hypoglycemia as well as exogenous corticotropin releasing hormone (CRH) produce a rise in serum BE since BE, beta-lipotropin and ACTH come from the common precursor proopiomelanocortin (POMC). This paper intended to evaluate the curve of serum BE concentration during such a test in uremic patients on hemodialytic treatment. 13 patients with CRF hemodialysed 4 to 38 months (mean: 17 months) and 14 healthy subjects were examined. In each of them crystalline insulin (0.1 units/kg of body mass) was given intravenously and blood samples were collected every 30 minutes. BE concentration was measured by radioimmunoassay without previous chromatographic separation. The test was performed after an overnight rest in the morning in persons staying at the recumbent position. An adequate hypoglycemia was obtained in every subject. Basal serum BE concentration was significantly higher in patients with CRF than in healthy subjects and correlated positively with duration of hemodialytic treatment. After 60 min. from insulin injection in both groups the peak BE level was observed whereas after 120 min. in returned to the initial values. The curve of BE concentration in patients with CRF ran on a significantly higher level than in healthy subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Pol Arch Med Wewn 1993 Mar
PMID:[Levels of beta-endorphin in serum of patients with chronic renal failure treated with hemodialysis during a test which stimulates hypoglycemia after insulin]. 832 71

There are three classes of endogenous opioid peptides: endorphins, enkephalins, dynorphins. Beta-endorphin is the main representative of endogenous opioid peptides. Beta-endorphin plays a role in the regulation of the normal menstrual cycle and possibly in the onset of puberty. This peptide is also involved in the pathophysiology of such menstrual disorders as: exercise-associated amenorrhoea, stress-induced amenorrhoea, weight loss related amenorrhoea and premenstrual syndrome. Probable mechanism is that alterations in the levels of beta-endorphin may change the pulsatile release of GnRH. This article reviews contemporary views on the role of beta-endorphin in the physiology and disorders of the menstrual cycle.
Ginekol Pol 1995 Oct
PMID:[Beta-endorphin--physiologic role and menstrual cycle disorders]. 868 45

Levels of beta-endorphin, FSH, LH, PRL, cortisol and estradiol in blood serum were measured in 20 girls with weight loss related amenorrhoea. Serum beta-endorphin levels were also measured in a group of 15 young, regularly menstruating healthy girls (control group). Levels of beta-endorphin were significantly lower in examined group than in control one. Serum levels of FSH, LH, estradiol were low. Serum levels of PRL and cortisol were normal. These observations suggest, that beta-endorphin is involved in the pathogenesis of weight loss related amenorrhoea.
Ginekol Pol 1995 Oct
PMID:[Evaluation of beta-endorphin levels and gonadotropin, prolactin, cortisol and estradiol in serum of girls with secondary amenorrhea associated with weight loss]. 868 46

Adenosine deaminase (ADA) activity was studied in red blood cells of patients suffering from multiple sclerosis treated with adrenocorticotropic hormone (ACTH). ADA activity in hemolysates was determined according to the method of Hopkinson and calculated as units per g of hemoglobin. Activity of adenosine deaminase in healthy subjects was 0.871 +/- 0.251 U/g Hb. In patients with multiple sclerosis, before treatment ADA activity was 0.765 +/- 0.131 U/g Hb and was about 15.2% lower than in the control group (p < 0.02). After treatment with ACTH, ADA activity increased to 1.005 +/- 0.211 U/g Hb (p < 0.001). We have suggested that increased activity of adenosine deaminase in red blood cells of patients suffering from multiple sclerosis after treatment with ACTH is caused by diminution of superoxide generation, and therefore its sparing effect on cell membrane and enzyme is connected with membranes.
Pol J Pharmacol
PMID:Activity of adenosine deaminase in red blood cells of patients suffering from multiple sclerosis treated with adrenocorticotropic hormone. 886 75

A review of the literature has been presented concerning pathogenetic role of limbic-hypothalamic-pituitary-adrenal axis (LHPA) in depression and the therapeutic possibility obtained by influencing this axis. Increased cortisol concentration has until now been the best documented biochemical abnormality in depression. Pathological results of the Dexamethasone Suppression Test pointing to hyperactivity of LHPA axis are found in about half of depressive patients. According to most recent research, primary disturbance of LHPA axis concerns hypothalamus (excessive secretion of corticotropin releasing factory) and limbic system (insufficiency of glucocorticoid receptor). An association was found between disturbances of LHPA axis in depression and immune system abnormalities in this illness. Disturbances of serotonergic and noradrenergic neurotransmission in depression may also partially result from LHPA axis dysfunction. In recent years, the attempts have been made to use drugs acting on LHPA axis for therapeutic purposes in depression, such as ketoconazole, within the framework of antiglucocorticoid strategy. Influencing LHPA axis may underlie the mechanism of new antidepressant drug, tianeptine. Recently, it was found that classical tricyclic antidepressant drugs as well as electroconvulsive may also act on LHPA in regulatory way.
Psychiatr Pol
PMID:[Limbic-hypothalamic-pituitary-adrenal axis in depression: literature review]. 898 15

The influence of adrenocorticotropic hormone (ACTH) and prednisone on the effects of amitriptyline (AMI), imipramine (IMI), mianserin (MIA) or nomifensine (NOM) was investigated in forced swimming and in open field tests. ACTH (50 I.U./kg) or prednisone (1 mg/kg) were given in a single dose or for 7 consecutive days alone or together with AMI (10 mg/kg), IMI (10 mg/kg), MIA (10 mg/kg) or NOM (2 mg/kg). It was found that neither ACTH nor prednisone administered alone in a single dose or for 7 days influenced the behavior of rats. ACTH co-administered with AMI or NOM in a single dose or with AMI, IMI or NOM for 7 days potentiated the antiimmobility effect of antidepressant drugs. Prednisone potentiated only antiimmobility effect of NOM in forced swimming test. ACTH as well as prednisone co-administered with NOM (but not with the other drugs), in a single dose as well as for 7 days, increased also locomotor activity in open field. Neither ACTH nor prednisone influenced the effect of MIA in both tests used. It was concluded that the specific synergism exists only between ACTH and tricyclic antidepressants (AMI, IMI). The observed behavioral interaction between ACTH and AMI or IMI does not seem to be mediated by adrenocorticoids (prednisone was without effect). The potentiation of NOM effects by ACTH as well as by prednisone and lack of any interaction with MIA seems to be related with different mechanism of action of those antidepressant drugs.
Pol J Pharmacol
PMID:Studies on the interaction of antidepressant drugs with adrenocorticotropic hormone or prednisone in rats. 911 44

The objective of this study was to analyse the effects of isoflurane anesthesia (lasting for 15 or 60 min) and isoflurane anesthesia termination (after 1 or 24 h) on met-enkephalin (MENK) and leu-enkephalin (LENK) levels in discrete brain areas and spinal cord segments in rabbits. Moreover histochemical analysis of activities of succinate dehydrogenase, magnesium-dependent adenosine triphosphatase (Mg++ATP-ase) and acid phosphatase in the striatum and hypothalamus were carried out to evaluate the effects of isoflurane anesthesia on energetic, transport and catabolic processes. Throughout anesthesia (15 and 60 min) and after its termination (1 h) the LENK contents were increased in hypothalamus, hippocampus, mesencephalon and lumbar segment of spinal cord. Moreover, during isoflurane anesthesia and after its termination (1 h) MENK and LENK levels decreased in cervical segment and MENK content dropped in thoracic segment of spinal cord. Histochemical data indicated, that isoflurane enhanced energetic processes as well as exchange processes in neurocytes, glial cells, capillary walls and ependymal cells of the third ventricle. Measurements of acid phosphatase activity provided evidence of no signs of toxicity of isoflurane in the examined areas. The changes in enkephalin levels observed during the isoflurane anesthesia and after its termination depended on the type of examined neuropeptides, as well as on parts of the brain and spinal cord studied. The changes observed after isoflurane administration in enkephalinergic system are discussed with regard to our earlier experiments with halothane and enflurane.
Pol J Pharmacol
PMID:Influence of isoflurane on enkephalin levels and on some indicatory enzymes in the central nervous system of rabbits. 943 56


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