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)

Untrained, moderately trained (runners, 15 to 25 mi/wk), and highly trained (runners, greater than 45 mi/wk) men participated in graded treadmill exercise at 50%, 70%, and 90% of their maximal oxygen consumption to quantify the relation between intensity of exercise and sympathetic nervous system and metabolic responses. Sympathetic system activation was noted at all intensities tested and was proportional to the relative exercise intensity. The magnitudes of the norepinephrine (NE) and epinephrine (E) responses were similar in all three groups of men at each relative exercise intensity and correlated with the magnitudes of change in levels of circulating plasma adrenocorticotropin hormone, cortisol, lactate (La), phosphate (Pi), and glucose (GI). The magnitudes of change in concentrations of La, Pi, and GI were also similar for the three groups at each relative exercise intensity. In contrast, a lower degree of sympathetic system activation in response to a given absolute workload was noted in the moderately and highly trained men as compared to that of the untrained men. Sympathetic and metabolic responses to exercise are similar under conditions of comparable relative exercise intensities, regardless of conditioning level. The sympathetic-adrenal medullary system is more sensitive to exercise than the hypothalamic-pituitary-adrenal axis. For a given absolute workload, the degree of activation significantly lower in trained individuals.
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PMID:Hormonal and metabolic responses of untrained, moderately trained, and highly trained men to three exercise intensities. 253 58

In a 49-year-old woman with empty sella syndrome, corticotropin (ACTH) deficiency and various abnormalities, including increased thyrotropin (TSH) secretion, growth hormone (GH) deficiency, and inappropriately high insulin with early phase hypoglycemia, during an oral glucose tolerance test were found. Existence of serum antipituitary antibody suggested that the empty sella and ACTH deficiency may be caused by an autoimmune destruction of the pituitary gland. All of the accompanying abnormalities except for increased TSH secretion were corrected with glucocorticoid supplement. Thyroidal responses to an increase and decrease of endogenous TSH were qualitatively normal, indicating that the patient's TSH was biologically active and the set point of hypothalamic-pituitary feedback regulation for TSH secretion was shifted.
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PMID:ACTH deficiency and TSH hypersecretion in a patient with empty sella turcica. 253 55

Changes in the blood and the behaviour of 14 growing pigs from 4 different litters were evaluated under different experimental conditions of blood sampling, grouping and adrenal stimulation. The results showed that the different techniques of blood sampling influenced lactic dehydrogenase (LDH) and creatine kinase (CK) activities. Cortisol, proteins and CK levels were negatively correlated with social hierarchy after regrouping. Cortisol was also correlated with total activity levels. Adrenal stimulation by adrenocorticotropic hormone (ACTH) administration caused a sharp increase in plasma cortisol levels. However, plasma glucose, plasma proteins and total leukocyte counts were not affected by the ACTH treatment.
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PMID:Effects of blood sampling procedures, grouping and adrenal stimulation on stress responses in the growing pig. 253 97

Previous studies have indicated that motor center ("feedforward") activity is important for hormonal and metabolic responses to exercise. Now, epidural blockade at vertebrae L3-L4 was used to evaluate the importance of afferent neural feedback from working muscles. Six healthy, young males cycled for 20 min at 55 +/- 4% (mean +/- SE) of maximal oxygen uptake with, as well as without, epidural anesthesia. During anesthesia cutaneous sensory blockade was present below segment T11-12, the postexercise ischemic pressor response was attenuated from 34 +/- 9 to 14 +/- 4 mmHg, muscle strength reduced to 80 +/- 5% of control, and perceived exertion (Borg scale) was increased. At rest hormonal and metabolic parameters did not change in response to epidural anesthesia. During exercise, responses of catecholamines, insulin, glucagon, and growth hormone (GH) in plasma as well as glucose production and utilization, plasma free fatty acids, and plasma glycerol were similar in epidural and control experiments (P greater than 0.05). In contrast during submaximal exercise, plasma concentrations of adrenocorticotropin (ACTH) and beta-endorphin increased only in experiments without epidural anesthesia. The data indicate that impulses in afferent nerves from the working muscles are essential for the ACTH and beta-endorphin responses to submaximal dynamic exercise in humans. Afferent nervous activity is probably less important than efferent activity from motor centers for responses of GH, catecholamines and insulin, and, in turn, extramuscular fuel mobilization in exercise.
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PMID:Hormonal and metabolic responses to exercise in humans: effect of sensory nervous blockade. 254 39

These experiments were designed to test whether the pattern of change in plasma corticosteroid or the total corticosteroid dose is important in determining the degree of inhibition of adrenocorticotropic hormone (ACTH) responses to stress by corticosteroid intermediate-delayed feedback. Five conscious dogs were studied. The ACTH response to induced hypoglycemia was measured after no prior corticosteroid feedback signal or after a corticosteroid feedback signal produced by infusion, two bolus injections, or three bolus injections of cortisol and corticosterone. The total corticosteroid dose (45 micrograms/kg) and the total interval of steroid treatment (60-30 min before hypoglycemia) were the same in all three cases of corticosteroid treatment. Changes in plasma glucose concentration during induced hypoglycemia were not altered by corticosteroid treatment. The plasma ACTH response to hypoglycemia was inhibited by all three patterns of treatment with corticosteroids. The inhibition of ACTH response was not significantly altered among the patterns of treatment with corticosteroids. The data suggest that the integrated (total) or the mean change in plasma corticosteroid concentration over time determines the degree of inhibition of stimulated ACTH in this time domain.
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PMID:Control of canine ACTH by corticosteroids: an integral feedback effect of steroids. 254 11

The present studies were undertaken to characterize further the influence of synthetic human beta-endorphin (0.5 mg/h) on insulin and glucagon responses to intravenous glucose in humans. Infusion of beta-endorphin in 10 normal volunteers caused a clear-cut inhibition of the overall insulin responses to a glucose pulse (0.33 g/kg iv) with values of glucose disappearance rates in the diabetic range [0.89 +/- 0.09 (P less than 0.01) vs. saline 1.82 +/- 0.15%/min]. Glucose-induced glucagon suppression was significantly lower during beta-endorphin, a fact that could have contributed to the reduced glucose utilization rates. The infusion of theophylline (150 mg + 350 mg/h) to increase the intracellular cAMP activity by inhibiting phosphodiesterase completely reversed the inhibitory effect of beta-endorphin on glucose-induced insulin secretion. As a consequence, glucose disappearance rates rose to 1.77 +/- 0.18%/min. Theophylline did not influence significantly the glucagon-releasing effect of beta-endorphin as well as the reduced glucagon suppression. An infusion of exogenous calcium (100 mg as iv bolus + 5 mg/min) to raise serum calcium in the hypercalcemic range (15 mg/dl) and lysine acetylsalicylate (72 mg/min) to block the synthesis of endogenous prostaglandin E did not interfere with the inhibiting effect of beta-endorphin on insulin secretion. These data confirm that beta-endorphin stimulates glucagon and inhibits basal and glucose-stimulated insulin secretion and suggest that the opioid influences the intraislet adenylate cyclase activity.
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PMID:Beta-endorphin and islet hormone release in humans: evidence for interference with cAMP. 255 Nov 76

This study was designed to assess effects of exercise on plasma and cerebrospinal fluid (CSF) levels of immunoreactive (ir) beta-endorphin, ACTH, cortisol, norepinephrine, and glucose in the conscious dog. Dogs were exercised on a treadmill at low or high intensity (4.2 miles/h and a 6% or 20% incline) for 90 min, and were allowed to recover for 90 additional min. Neither intensity of exercise changed plasma glucose levels, but dose-related changes in glucose kinetics did occur. CSF glucose declined in both groups. During low intensity exercise, plasma levels of ir-beta-endorphin, ACTH, and cortisol increased with duration of exercise. During high intensity exercise, ACTH, ir-beta-endorphin and cortisol increased faster, and the integrated plasma response of these hormones was greater. Thus, peripheral release of ir-beta-endorphin, ACTH, and cortisol during exercise is dose-related with respect to time and intensity. CSF ir-beta-endorphin and ACTH both increased during low- but not high-intensity exercise. CSF cortisol rose markedly in both exercise groups. During high-intensity exercise there was a 50% increase in CSF norepinephrine, indicating that exercise induces alterations in central noradrenergic turnover. We conclude that exercise is a physiologic regulator of both peripheral and central neuroendocrine systems.
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PMID:Effects of low- and high-intensity exercise on plasma and cerebrospinal fluid levels of ir-beta-endorphin, ACTH, cortisol, norepinephrine and glucose in the conscious dog. 255 59

To find out whether the hippocampus is involved in central nervous system-mediated glucoregulation, we injected saline, neostigmine, dopamine, norepinephrine, bombesin, beta-endorphin, somatostatin, and prostaglandin F2 alpha into the dorsal hippocampus in anesthetized fed rats. After injection of dopamine, norepinephrine, bombesin, beta-endorphin, somatostatin, or prostaglandin F2 alpha, the level of hepatic venous plasma glucose did not differ from that in saline-treated control rats. However, neostigmine, an inhibitor of acetylcholine esterase, caused a dose-dependent increase in the hepatic venous plasma glucose concentration. This neostigmine-induced hyperglycemia was dose-dependently suppressed by coadministration of atropine, but not by hexamethonium. Injection of neostigmine (5 X 10(-8) mol) resulted in an increase not only in glucose but also in glucagon, epinephrine, and norepinephrine in hepatic venous plasma. In bilateral adrenalectomized rats, neostigmine-induced hyperglycemia was suppressed, but the hepatic venous plasma glucose concentration still increased significantly. These results indicate that the hippocampus is involved in central nervous system-mediated glucoregulation through cholinergic muscarinic activation, partly via epinephrine secretion.
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PMID:Involvement of the hippocampus in central nervous system-mediated glucoregulation in rats. 256 20

Since opioid peptides and opiate receptors have been demonstrated in the pancreatic islets, we investigated the effects of beta-endorphin, met-enkephalin, and dynorphin A, on basal and stimulated insulin secretion in the mouse. Each of the three opioid peptides was injected intravenously (0.06-64 nmol/kg) alone or together with each of the three insulin releasing agents glucose (2.8 mmol/kg), carbachol (cholinergic agonist, 0.16 mumol/kg), or terbutaline (beta 2-adrenoceptor agonist, 3.6 mumol/kg). It was found that beta-endorphin, met-enkephalin, and dynorphin A were all without effect on basal plasma insulin levels, except a slight elevation by beta-endorphin induced at 2 min after its injection at 64 nmol/kg (to 41 +/- 2 microU/mL vs 28 +/- 4 microU/mL in controls; p less than 0.05). Glucose- and terbutaline-induced insulin secretion were inhibited by beta-endorphin at the lower dose levels of 0.25 (p less than 0.01) and 1 nmol/kg (p less than 0.05). This effect was counteracted by the opiate receptor antagonist naloxone (500 micrograms/kg). In contrast, beta-endorphin at the high dose levels of 16 and 64 nmol/kg augmented the glucose- and terbutaline-induced insulin secretion (p less than 0.05). Carbachol-induced insulin secretion was not affected by beta-endorphin at the lower dose levels but augmented by the peptide at 64 nmol/kg (p less than 0.01). Met-enkephalin inhibited glucose- (p less than 0.01) and terbutaline- (p less than 0.05) induced insulin secretion at the high dose rates of 16 and 64 nmol/kg, but the peptide was without effect on carbachol-induced insulin secretion. The inhibitory effects were counteracted by naloxone. Dynorphin A did not affect stimulated insulin secretion at any of the dose levels tested. In summary, in the mouse 1. beta-Endorphin at low dose levels inhibits and at high dose levels augments stimulated insulin secretion; 2. Met-enkephalin inhibits stimulated insulin secretion; and 3. Dynorphin A does not affect insulin secretion. It is suggested that the main influence of beta-endorphin and met-enkephalin under in vivo conditions in the mouse is to inhibit stimulated insulin secretion.
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PMID:Effects of beta-endorphin, met-enkephalin, and dynorphin A on basal and stimulated insulin secretion in the mouse. 257 36

The effect of the antipsychotic peptide, Org 5878 (desenkephalin-gamma-endorphin, beta-endorphin-(6-17), on local cerebral glucose utilization was studied in freely moving male Wistar rats. Org 5878 (20 micrograms/kg, i.v.) or saline were given acutely and local cerebral glucose utilization was measured in 116 brain structures. Glucose uptake was not altered by Org 5878 in most brain areas, including areas of the nigrostriatal system, the cortex and the thalamus. However, significant reductions in glucose uptake were observed in the ventral tegmental area, the diagonal band complex, the hippocampus, the amygdala, the interpeduncular nucleus, the reticular nucleus of the thalamus and the cerebellum. These results indicate that the nigrostriatal and cortico-thalamic systems remain unaffected but the activity of the mesolimbic ventral tegmental area and of major target areas of cholinergic basal forebrain structures is selectively reduced following Org 5878 administration. It is concluded that the effect of Org 5878 on local cerebral glucose utilization is distinct from and more selective than that of antipsychotics currently used in the clinic.
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PMID:The neuropeptide, Org 5878 (desenkephalin-gamma-endorphin, DE gamma E), affects local cerebral glucose utilization in freely moving rats. 257 30


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