Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of centrally administered beta-endorphins on glucose homeostasis in the conscious dog were studied. Intracerebroventricular administration of beta-endorphin (0.2 mg/h) caused a 70% increase in plasma glucose. The mechanism of the hyperglycemia was twofold: there was an early increase in glucose production and a late inhibition of glucose clearance. These changes are explained by marked increases in plasma epinephrine (30-fold) and norepinephrine (6-fold) that occurred during infusion of beta-endorphin. Central administration of beta-endorphin also resulted in increased levels of adrenocorticotropic hormone and cortisol. In addition there was an increase in plasma insulin but no increase in plasma glucagon. Intravenous administration of beta-endorphin did not alter glucose homeostasis. Intracerebroventricular administration of acetylated beta-endorphin did not perturb glucose kinetics or any of the hormones that changed during infusion of the unacetylated peptide. We conclude that beta-endorphin acts centrally to cause hyperglycemia by stimulating sympathetic outflow and the pituitary-adrenal axis. Acetylation of beta-endorphin abolishes the in vivo activity of the peptide.
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PMID:Central effects of beta-endorphins on glucose homeostasis in the conscious dog. 252 86

Numerous studies have shown a rise of blood sugar concentrations and serum levels of pancreatic polypeptides after pharmacological doses of beta-endorphin. We tested the yet unknown influence of physiological fluctuations in beta-endorphin serum levels on glucose homeostasis by stimulating the pituitary secretion with CRF. 100 micrograms of human CRF or saline solution were intravenously injected in ten healthy male subjects at least one week apart. beta-endorphin serum levels rose significantly after the injection of CRF, but there was no change in blood sugar concentrations or serum levels of glucagon or insulin at all. We conclude that only a pharmacological dose of beta-endorphin influences glucose homeostasis.
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PMID:Increase of beta-endorphin serum levels by human corticotropin-releasing factor does not affect beta-cell function in normal-weight men. 252

The present study was designed to examine the role played by beta-endorphin in the physiological response to the stress of insulin-induced hypoglycemia. Three groups (n = 5, each) of conscious overnight-fasted dogs, chronically fitted with catheters in the femoral artery and in the third ventricle were used for these studies. Each experiment consisted of an 80-min equilibration period (0-80 min), a 40-min basal period (80-120 min), and a 180-min (120-300 min) experimental period. One group received a 220-min intracerebroventricular (icv) infusion of naloxone (0.2 mg/h) beginning at t = 80 min. The second group received a 3-h intravenous infusion of insulin at 5.0 mU.kg-1.min-1 beginning at t = 120 min. The third group received naloxone at t = 80 min and insulin beginning at t = 120 min, and both were continued throughout the experimental period. The studies show that insulin-induced hypoglycemia was associated with a rise in plasma cortisol, beta-endorphin, epinephrine, norepinephrine, and glucagon. Pretreatment with naloxone diminished the rises in plasma beta-endorphin, epinephrine, and norepinephrine without affecting the responses of plasma glucagon and cortisol. Although the levels of hypoglycemia achieved in the two groups were identical, glucose rates of appearance into and disappearance from the plasma compartment were higher in the group pretreated with icv naloxone (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of naloxone on glucose homeostasis during insulin-induced hypoglycemia. 252 11

Developmental patterns for rat pancreatic opioid peptides and islet hormones were studied from gestational day 20 through adulthood. Fetal tissue was obtained as well as pancreas at birth (day 0), and postnatal days 3, 7, 14, and 21, and 7 weeks. The hormones measured included insulin, glucagon, and somatostatin. The opioids measured were beta-endorphin, Met- and Leu-enkephalins, and the high molecular weight enkephalin precursors. Pancreata were pooled as necessary and extracted (acid alcohol, or hot acetic acid), and opioids were further purified on reversed-phase C-18 (Sep-pak) cartridges. In all instances measurements were made by radioimmunoassays. Precursor peptides were first digested (with trypsin and carboxypeptidase B) prior to immunoassay. All opioids and hormones except the precursors for enkephalins showed a well-defined surge in pancreatic concentration during the first postnatal week. In contrast, the precursors had the highest concentration in the fetus, and by the seventh day of life had decreased by greater than 50%. This progressive decrease may represent maturation of the enkephalin convertase and trypsin-like enzymes in the islets. The opioid and hormonal surges that we have described are similar to the surge in islet concentration of thyroid-releasing hormone (TRH) previously described in neonatal rat islets. It is suggested that these postnatal alterations in opioid and hormone concentration relate to a specific function in the development of the endocrine pancreas.
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PMID:Developmental patterns for pancreatic opioids in the rat. 253 May 76

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

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

Thyroid hormones are required for maximal stimulation of lipolysis of fat cells by catecholamines corticotropin and glucagon. Several reasons have been given to explain this fact, but all of them are controversial and still not definitive. It has been proposed that adenosine is an important factor in the low lipolytic response to catecholamines by fat cells of hypothyroid rats. This proposal has been studied with corticotropin. There has been no recuperation of maximal lipolysis when fat cells of hypothyroid rats were stimulated by corticotropin in the presence of adenosine deaminase.
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PMID:Lipolysis by corticotropin in fat cells from hypothyroid rats. Effect of adenosine deaminase. 256 27

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

The PAP technique was used to examine adult human pancreata (corpus) immunohistochemically for the presence of beta-endorphin containing cells. These cells were found to account for 4.8% of the islet cells. They are irregularly distributed within the islets, where they occur singly or in groups of 3 to 5 cells between the acini (0.4% of the parenchyma). Investigations designed to detect the simultaneous presence of beta-endorphin and somatostatin or glucagon revealed that beta-endorphin occurs in somatostatin cells (1.0% of the islet parenchyma). This is the 1st proof that these 2 hormones appear together. The simultaneous presence of beta-endorphin and glucagon in the same cell was also observed in 0.9% of the islet parenchyma. Earlier studies undertaken by us have shown that beta-endorphin is synthetized in the islets of Langerhans. Possible functions of beta-endorphin in the islets are discussed.
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PMID:Immunohistochemical investigations of beta-endorphin in human pancreatic islets. 256 68

Culturing sympathetic ganglion neurons in vitro may modify phenotypic expression of some neurotransmitters. For dorsal root ganglia (DRG), contradictory results have been reported; most studies have used immature material. We have therefore performed a detailed immunocytochemical analysis of the transmitter content of cultured adult rat DRG neurons. To demonstrate possible modifications of neurotransmitter phenotypes, we have compared the results obtained with the same techniques on neurons cultured for 3 days and on freshly dissociated DRG cells. Also, the transmitter profile of cultured neurons was compared with that known from in situ studies. Out of 22 antigens studied, 20 were detected in cultured DRG neurons. All of them were expressed in small and/or intermediate-sized cells. Large neurons only contained CGRP, VIP, NPY, beta-END, ENK, and GABA. The percentage of immunostained neurons varied for the various antisera: less than 10% of cultured neurons were positive for ENK, beta-LPH, beta-END, DYN, VASO, and OXY; 10-30% for SOM, CCK, CAT, and SP; and greater than 30% for NPY, CRF, GLU, NT, VIP, GABA, GRP, CGRP, 5-HT, and TRH. In the latter two groups of transmitters (except CGRP), the proportion of immunoreactive neurons was by far larger in cultured than in freshly dissociated DRG. The most pronounced (greater than 25%) increase in the proportion of positively stained neurons after culturing was observed for the GRP, CRF, TRH, and 5-HT antisera. Serotonin was the only transmitter identified in cultured but not in freshly dissociated cells. These data indicate, on one hand, that various antigens, for example, CAT, GABA, NT, TRH, NPY, beta-LPH, and beta-END, which up to now have not been described in DRG in situ, can be detected immunocytochemically a few hours after dissociation of adult rat DRG. On the other hand, several transmitters, for example, VIP, NPY, SP, GABA, GLU, NT, GRP, CRF, TRH, and 5-HT, are expressed in a significantly higher proportion of cells in cultured than in freshly dissociated preparations. This might reflect a change in the phenotypic expression of transmitters due to the new environment generated by the culture conditions, a hypothesis that can be tested by measuring specific mRNA levels. Moreover, considering the plasticity and multipotentiality of their transmitter phenotype, cultured adult DRG neurons might represent an interesting material for autografts into the injured central nervous system.
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PMID:Neurotransmitter phenotype plasticity in cultured dissociated adult rat dorsal root ganglia: an immunocytochemical study. 256 40


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