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)

We investigated the effects of sevoflurane anesthesia and of surgery, on the endocrine functions as reflected by plasma levels of cortisol, aldosterone, ACTH, beta-endorphin-like immunoreactivity, prolactin, insulin, growth hormone, glucagon and glucose in surgical patients.
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PMID:Endocrine evaluation of sevoflurane, a new inhalation anesthetic agent. 262 72

Information on equine stress responses to anaesthesia and surgery is sparse. Six ponies were anaesthetized for 2 h with halothane and no surgery was performed. Plasma concentrations of glucose, lactate, non-esterified fatty acids, cortisol, insulin, catecholamines and adrenocorticotropic hormone (ACTH) were measured. The results were compared with those obtained in the same group of ponies over the same time period on a different day with the animals conscious. Anaesthesia induced an increase in plasma concentrations of glucose, lactate, cortisol and ACTH and a decrease in plasma concentration of insulin. The response was the same when the study was repeated 18 months later. This suggests that anaesthesia alone, with a commonly used clinical technique, induced a substantial stress response in the horse. More benign anaesthetic techniques should be sought in this species.
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PMID:Equine stress responses to anaesthesia. 269 73

Corticotropin releasing factor (CRF) has been administered into the third ventricle of lean and genetically obese Zucker fatty rats in both acute and chronic experiments. Following a single injection of CRF (5 micrograms or approximately 1 nmole) there was an acute reduction of food intake in both the lean and obese animals, but the effect was greater in the obese. This effect persisted for the first three hours but was no longer detectable in either lean or genetically obese animals at 6 hours. Binding of GDP to mitochondria from interscapular brown adipose tissue in 21-hour deprived animals was lower in the fatty rats than in the lean controls. The injection of CRF significantly increased GDP binding in both the lean and fatty rats. During chronic infusion of CRF into the third ventricle of fatty rats, there was a significant decrease in food intake in the obese rats and fall of body weight in both groups. The basal levels of GDP binding were significantly lower in the saline-infused fatty rats than in the saline-infused lean controls. The chronic infusion of CRF increased GDP binding in the fatty rats but not in the lean animals. The CRF-treated values for GDP binding in fatty rats however, remained significantly below the baseline values in the control animals. Chronic CRF infusion also significantly lowered glucose levels in the fatty rat. These studies are consistent with the hypothesis that CRF may be involved in the decreased food intake and increased sympathetic activity observed in genetically obese fatty rats following adrenalectomy.
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PMID:Effects of corticotropin releasing factor on genetically obese (fatty) rats. 278 15

Products of the pro-opiomelanocortin gene have been shown to have marked effects on insulin secretion. Selective antagonists of beta-endorphin have been reported to correct the impaired insulin secretory response to glucose seen in non-insulin dependent diabetes. Families with an autosomal dominant pattern of inheritance of diabetes were studied for possible linkage between diabetes and the pro-opiomelanocortin locus by examining the inheritance of a Rsa 1 restriction fragment length polymorphism. In two families with classical Type 2 diabetes there were recombinants between the disease and the pro-opiomelanocortin locus. In a family with maturity-onset diabetes of the young there were only two informative meoises, but there was a crossover between the disease and the pro-opiomelanocortin gene locus. Inherited defects in or near the pro-opiomelanocortin gene locus are unlikely to be directly involved in the aetiology of non-insulin dependent diabetes.
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PMID:Analysis of the pro-opiomelanocortin gene in non-insulin dependent diabetic families. 280 86

The study evaluated the hypothesis that during exercise autonomic neuroendocrine activity and, in turn, substrate mobilization, is subjected to feed-forward stimulation from motor centers. Eight young healthy men bicycled for two 20-min periods without (control, C) as well as during partial neuromuscular blockade with tubocurarine (Cu). 3-[3H]glucose was infused, and arterialized hand vein blood was sampled. In period 1 O2 consumption (VO2) (56% VO2 max), heart rate, and blood lactate were identical in Cu compared with C experiments, whereas hand grip strength was lower and perceived exertion [14.0 +/- 1.5 vs. 9.1 +/- 1.2 (SE) points, P less than 0.01] higher in Cu experiments, indicating higher motor center activity. Concentrations of norepinephrine [7.39 +/- 1.18 (Cu) vs. 5.14 +/- 1.06 (C) nmol/l], epinephrine (1.69 +/- 0.33 vs 0.87 +/- 0.16 nmol/l), growth hormone (25.9 +/- 7.3 vs. 11.5 +/- 4.7 mU/l), and adrenocorticotropin hormone (11.3 +/- 1.3 vs. 5.5 +/- 0.7 pmol/l) attained higher values in Cu than in C experiments (P less than 0.05). The initial increase in glucose production was enhanced in Cu (8.1 +/- 1.6 mumol.min-1.kg-1) compared with C experiments (3.9 +/- 1.9, P less than 0.05), and plasma glucose only increased in Cu experiments. Free fatty acid (P less than 0.05) and glycerol (P less than 0.1) concentrations were higher in Cu than in C experiments. In period 2 identical perceived exertion was achieved in the two experiments by reducing work load in Cu experiments. In this period hormonal responses were similar in the two experiments.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of motor center activity for hormonal changes and substrate mobilization in humans. 282 45

Intracisternal administration of synthetic human beta-endorphin to conscious, ambulatory adult male rats caused dose-related increases in plasma glucose concentration. The largest dose of beta-endorphin examined, 7.25 nmol, increased plasma glucose concentration within 7 min and this effect lasted 2.5 h. On the other hand, only 58 pmol was required to induce transient hyperglycemia, when compared to the response observed in saline-injected control rats. This hyperglycemic effect of beta-endorphin was prevented by prior systemic administration of naloxone, thus supporting the hypothesis that this beta-endorphin-induced effect is mediated at opioid receptors. beta-Endorphin also markedly increased plasma concentrations of epinephrine, norepinephrine and, to a lesser extent, dopamine. A significant positive correlation was demonstrated between plasma glucose and plasma epinephrine responses to increasing doses of intracisternally administered beta-endorphin. In addition, intracisternal beta-endorphin also increased plasma glucagon concentration without significantly increasing plasma insulin concentration. Thus, it is probable that epinephrine and glucagon are the major factors mediating this hyperglycemic effect. beta-Endorphin-induced hyperglycemia was prevented by ganglionic blockade with chlorisondamine. This further supports the thesis that intracerebral beta-endorphin increases plasma glucose concentration by activation of the central autonomic outflow. In addition to these effects on short-term regulators of glycemia, intracisternal beta-endorphin increased plasma concentrations of corticosterone and growth hormone. Both of these glucose counterregulatory hormones may play minor roles in modulating beta-endorphin-induced hyperglycemia.
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PMID:Autonomic and endocrine participation in opioid peptide-induced hyperglycemia. 282 68

Beagle dogs were given saline, insulin or the dopamine antagonist, haloperidol, to examine peripheral concentrations of immunoreactive (ir)-pro-opiomelanocortin (POMC) peptides resulting from pars distalis or pars intermedia stimulation. Six beagles were given each test substance on separate occasions with and without dexamethasone pretreatment. Plasma was assayed directly for glucose, ir-ACTH, ir-alpha-MSH, cortisol and, after Sephadex G-50 Fine gel filtration chromatography, for ir-beta-lipotrophin (ir-beta-LPH) and ir-beta-endorphin (ir-beta-END) content. Injection of 0.5 units insulin/kg lowered (P less than 0.01) plasma glucose from 4.9 +/- 0.3 mmol/l (mean +/- S.D., saline controls) to 2.3 +/- 0.5 mmol/l, coincident with increasing ir-ACTH (9.5 +/- 3.1 to 106 +/- 54 pmol/l), cortisol (52 +/- 27 to 221 +/- 27 nmol/l), ir-beta-LPH (not detectable to 34 +/- 18 pmol/l) and ir-beta-END (not detectable to 52 +/- 22 pmol/l). Plasma ir-alpha-MSH concentrations were not affected by insulin. Pretreatment with dexamethasone abolished the ir-ACTH, cortisol, ir-beta-LPH and ir-beta-END increases in response to 0.75 units insulin/kg. Haloperidol (1 mg/kg) increased (P less than 0.01) plasma ir-ACTH (to 103 +/- 63 pmol/l), cortisol (to 243 +/- 11 nmol/l), ir-beta-LPH (to 16 +/- 6 pmol/l), ir-beta-END (to 136 +/- 73 pmol/l) and additionally raised ir-alpha-MSH (7 +/- 8 pmol/l in saline controls to 131 +/- 80 pmol/l after haloperidol).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential secretion of pro-opiomelanocortin peptides by the pars distalis and pars intermedia of beagle dogs. 283 53

1. Physical effort involves, along with an increase in the plasma concentration of beta-endorphin, profound adaptations of the circulation and the endocrine system. The effects of opioid antagonism on the responses of blood pressure, heart rate and several hormones to exercise were therefore studied in 10 normal men. They exercised in the supine position up to 33% and 66% of their maximal exercise capacity and received in a randomized double-blind cross-over protocol, either saline or naloxone (10 mg intravenously, followed by a continuous infusion of 10 mg/h). 2. Intra-arterial pressure and heart rate were continuously monitored, but were not affected by naloxone. 3. At rest, opioid antagonism produced a rise in plasma renin activity and in plasma adrenocorticotropin, cortisol and aldosterone, but only the stimulation of the two adrenocortical hormones differed significantly from the control experiments; at rest naloxone also prevented the fall in plasma adrenaline, which occurred with saline infusion. Furthermore, the exercise-induced rises in plasma angiotensin II, aldosterone, cortisol, noradrenaline and adrenaline were higher on naloxone than on saline, while a similar tendency was also present for the increases with exercise in plasma renin activity and plasma adrenocorticotropin. Neither at rest nor during exercise did opioid antagonism alter plasma lactate and glucose and serum insulin and growth hormone. 4. In conclusion, (1) endogenous opioids are not involved in the responses of blood pressure and heart rate to supine exercise; (2) at rest and during exercise, the endogenous opioids inhibit the secretion of adrenocorticotropin, aldosterone, cortisol, noradrenaline and adrenaline; (3) they also inhibit the plasma renin-angiotensin II system indirectly via the catecholamines.
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PMID:Effects of opioid antagonism on the haemodynamic and hormonal responses to exercise. 284 14

This study was designed to assess effects of insulin-induced hypoglycemia on plasma and cerebrospinal fluid (CSF) levels of immunoreactive (ir) beta-endorphins, adrenocorticotropin (ACTH), cortisol, norepinephrine, insulin, and glucose in the conscious, overnight fasted dog. Dogs received either an intravenous infusion of saline or insulin (5 mU/kg/min) for 3 h. Infusion of saline alone in conjunction with acute sampling of CSF caused no measurable perturbations of glucose homeostasis. Insulin infusion caused a 60% drop in both plasma and CSF glucose. Plasma levels of ir-beta-endorphins, ACTH and cortisol rose markedly. CSF levels of ir-beta-endorphins and ACTH also increased. While the magnitude of the increase was smaller than that in the plasma, it was greater than would be expected if crossover of the peptides from the plasma were the sole source of the increase. Hypoglycemia also induced elevations in CSF cortisol and insulin. In addition, there was a 45% decrease in CSF norepinephrine in spite of large elevations of norepinephrine in the plasma. We conclude that hypoglycemia is associated with marked changes in central as well as peripheral levels of neuroendocrine factors. The importance of these changes in mediating acute and long-term responses to hypoglycemia remains to be established.
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PMID:Effects of insulin-induced hypoglycemia on plasma and cerebrospinal fluid levels of ir-beta-endorphins, ACTH, cortisol, norepinephrine, insulin and glucose in the conscious dog. 285 80

The response of the sympathoadrenal system to hypoglycaemia of different etiology was studied in seven infants, aged 10-189 days. Five infants had hyperinsulinism secondary to nesidioblastosis or to a beta-cell adenoma of the pancreas, one infant had neonatal sepsis due to staphylococcal infection and one infant congenital growth hormone (HGH) and adrenocorticotropic hormone (ACTH) deficiency. In babies with hyperinsulinism, plasma noradrenaline increased from 0.29 +/- 0.03 to 0.61 +/- 0.09 ng/ml (P less than 0.01), whereas adrenaline increased only in three, but did not change in two babies. Increases in heart rate and blood pressure paralleled these changes. In hypoglycaemia due to congenital sepsis, noradrenaline increased from 0.39 to 1.64 ng/ml and adrenaline from 0.05 to 0.86 ng/ml. This was associated with marked haemodynamic changes. In congenital HGH and ACTH deficiency, the low basal plasma levels of noradrenaline (0.12 ng/ml) and adrenaline (0.01 ng/ml) remained unchanged in response to hypoglycaemia. Heart rate and blood pressure were unaffected. The sympathoadrenal system was activated by hypoglycaemia in all infants except in congenital HGH and ACTH deficiency. In contrast to adults, noradrenaline was the preferentially released catecholamine, suggesting an involvement of noradrenaline in glucose counter regulation in infancy.
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PMID:Sympatho-adrenal response to hypoglycaemia in infants. 285 Sep 15


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