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 administration of monosodium-L-glutamate (MSG) during the neonatal period is known to result in central nervous system lesions in the arcuate nucleus of the hypothalamus and the retina. Rodents so treated exhibit behavioral deficts and endocrinopathies including obesity, hypogonadism, hypothyroidism, pituitary atrophy, tail automutilation and diminished locomotor activity. Assessment of endocrine status revealed normal serum levels of glucagon, thyroid-stimulating hormone and luteinizing hormone, and diminished levels of thyroid hormones and growth hormone in MSG-treated rats. Prolactin levels were elevated in the glutamate-treated male rats. Within the brain hypothalamic levels of thyrotropin-releasing hormone, luteinizing hormone-releasing hormone, and somatostatin were unchanged. Measurement of neurotransmitters and neurotransmitter-related enzymes in individual hypothalamic nuclei derived from MSG-treated rats revealed normal levels of norepinephrine, serotonin and glutamic acid decarboxylase, but reduced levels of choline acetyltransferase and dopamine in the arcuate nucleus and median eminence. Histochemical methods for visualization of dopamine and acetylcholinesterase in the mediobasal hypothalamus confirmed these findings. The MSG-treated animals exhibited a normal diurnal rhythm of pineal serotonin N-acetyltransferase activity. These data indicate that the MSG-induced endocrine deficiency syndrome results at least partly from destruction of cholinergic and dopamingeric tuberoinfundibular systems in the hypothalamus.
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PMID:Models of neuroendocrine regulation: use of monosodium glutamate as an investigational tool. 3 35

The effects of pulsatile and nonpulsatile flow pattern on pancreas and liver blood flow were studied in nine dogs on cardiopulmonary bypass (CPB). Furthermore, plasma levels of glucose, insulin, glucagon, growth hormone, and cholinesterase were compared in 20 patients subjected to open heart surgery with either pulsatile or nonpulsatile perfusion. Impairment of liver and pancreas function was significantly greater at the end of CPB and 48 h afterwards with nonpulsatile flow as compared with the pulsatile flow pattern. A decrease of intestinal blood flow that was demonstrated in dogs subjected to nonpulsatile perfusion could at least in part be responsible for the difference in postoperative organ function observed in patients after CPB.
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PMID:[Comparative studies on pulsatile and continuous flow during extracorporeal circulation. Effects on liver function and endocrine pancreas secretion]. 45 49

The influence of cholinergic agonists on central nervous system (CNS) regulation of blood sugar homeostasis was studied in fasted rats. When carbachol, muscarine, bethanechol, methacholine, or neostigmine was injected into the third cerebral ventricle, it caused a dose-dependent increase in the hepatic venous plasma glucose concentration. However, in the case of 1,1-dimethylphenyl-4-piperazinium iodide (DMPP) or nicotine, the level of hepatic venous glucose did not differ from that of the saline-treated control rats. The increase in glucose level caused by neostigmine was dose-dependently suppressed by coadministration of atropine. These facts suggest that cholinergic activation of muscarinic receptors in the CNS plays a role in increasing hepatic glucose output. Injection of neostigmine (5 X 10(-8) mol), an inhibitor of cholinesterase, into the ventricle resulted in the increase of not only glucose, but also glucagon, epinephrine, and norepinephrine in the hepatic venous plasma. However, constant infusion of somatostatin through a femoral vein completely prevented the increase of glucagon after administration of neostigmine, although the increase of hepatic venous glucose and epinephrine levels were still observed. Neostigmine-induced increments in glucose did not occur in adrenalectomized rats. This suggests that the secreted epinephrine acts directly on the liver to increase hepatic glucose output.
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PMID:Mechanism of central hyperglycemic effect of cholinergic agonists in fasted rats. 287 43

Fed and 18-h fasted rats were given acute doses of either saline or the acetylcholinesterase inhibitor pinacolyl methylphosphonofluoridate (soman) 40, 60, or 80 micrograms/kg. After 30 min plasma samples were collected and assayed for glucose, insulin, glucagon, corticosterone, epinephrine and norepinephrine and the hypothalamus was isolated and assayed for acetylcholinesterase activity. Toxic sign scores were determined and they indicated that soman may be more toxic in the fasted rat. Soman-induced increases in corticosterone were observed in both fasted and fed rats; these levels were significantly higher in fasted rats given either soman or saline. Also, soman-induced increases in glucagon were more pronounced in fasted rats. Soman also caused an apparent dose-dependent increase in catecholamines and a decrease in hypothalamic acetylcholinesterase activity in both groups of rats. The expected lower insulin and glucose levels in the fasted rats were present in the saline-dosed animals and remained lower than fed rats after each dose of soman. This lack of soman-induced hyperglycemia may contribute to the toxicity of soman in fasted rats.
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PMID:Effects of the acetylcholinesterase inhibitor pinacolyl methylphosphonofluoridate (soman) on selected endocrine, glucose, and catecholamine levels in fasted and fed rats. 305 28

The effects of acute doses of soman (40, 60, or 80 micrograms/kg sc) in rats were evaluated for toxic symptoms as well as for changes in plasma levels of glucose, insulin, glucagon, corticosterone, norepinephrine, and epinephrine. The relationship between changes in these levels and depressed acetylcholinesterase activity in the hypothalamus was determined. Soman 40 micrograms/kg did not manifest significant changes in any of the parameters evaluated. However, both the 60 and 80 micrograms/kg doses of soman caused dose- and time-related increases in plasma levels of glucose, corticosterone, norepinephrine, epinephrine, and a depression of insulin. Many of these increases, as well as the severity of toxicity, appear to be inversely related to the hypothalamic acetylcholinesterase levels. The hyperglycemia following the higher doses of soman is likely due to the combined effects of elevated levels of corticosterone, catecholamines, possibly glucagon, and depressed insulin levels. Stress from the toxic effects of soman is likely partially responsible for the endocrine effects since most of the changes observed are consistent with changes in these levels that would be manifested in an animal stress model.
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PMID:Effect of acute soman on selected endocrine parameters and blood glucose in rats. 306 86

The effects of repeated administration of soman on plasma glucose levels, acetylcholinesterase (AChE) activity in erythrocytes and hypothalamus, and plasma levels of corticosterone, glucagon, insulin, epinephrine, and norepinephrine were studied in male rats. Rats were given soman subcutaneously (sc), either 30 micrograms/kg every 24 hr for 5 or 12 days or 40 micrograms/kg every 24 hr for 5 days. All doses of soman markedly depressed AChE activity in the hypothalamus and completely inhibited AChE activity in erythrocytes. Soman 30 micrograms/kg given for 5 days did not alter plasma levels of any hormone assayed and produced few signs of intoxication. Soman 40 micrograms/kg given for 5 days elevated plasma levels of glucose and corticosterone and produced signs of severe cumulative intoxication. Daily administration of 30 micrograms/kg of soman for 12 days inhibited hypothalamic AChE activity 75%, lowered plasma insulin, and produced signs of moderate intoxication. Repeated administration of soman produced endocrine alterations only when significant signs of intoxication were evident. The absence of increases in plasma levels of catecholamines and corticosterone in rats exhibiting signs of moderate intoxication, and of catecholamines in rats exhibiting signs of severe intoxication, may indicate an impairment by soman of the normal endocrine response to stress.
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PMID:Effect of repeated administration of soman on selected endocrine parameters and blood glucose in rats. 306 87

Autonomic innervation of the pancreas of the camel has been studied using histochemical techniques for the demonstration of adrenergic and cholinergic (acetylcholinesterase-positive) nerves. Both extrinsic and intrinsic innervation of the pancreas were found. Distinct peri-acinar, perivascular, peri-insular and periductal plexuses were found as well as both adrenergic and cholinergic ganglia. The role of the autonomic nerves in the synthesis and release of insulin, glucagon and somatostatin is discussed.
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PMID:A histochemical study on the innervation of the pancreas of the one-humped camel (Camelus dromedarius). 365 46

In 20 patients who underwent open-heart surgery, the plasma concentrations of glucose, insulin, glucagon, growth hormone, free hemoglobin, and cholinesterase were measured before, during and after pulsatile and continuous perfusion. Pulsatile flow was achieved by modification of a roller pump to effect rapid acceleration and slowing. The driving motor was interfaced with a control module to enable ECG-triggered perfusion. In addition to the clinical studies, investigations were performed in 9 dogs to assess the effects of pulsatile and continuous perfusion on liver and pancreas flow during total bypass. During pulsatile perfusion there was a significant increase in insulin which, however, was clearly diminished in relation to glucose levels. The response of the beta-cells was markedly more compromised after continuous than pulsatile perfusion. The secondary postoperative increase in insulin can be accounted for by intravenous administration of glucose and, particularly, after pulsatile perfusion, indicates an almost completely normal response of pancreatic beta-cells. As opposed to the effects of continuous perfusion, the low glucose, glucagon, and growth hormone levels, the insulin increase during and after pulsatile perfusion as well as normal cholinesterase values observed in association with pulsatile perfusion appear to be the result of improved pancreatic and hepatic function. This contention is supported by the experimental finding of significantly increased pancreas and liver perfusion during pulsatile perfusion.
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PMID:[Clinical and experimental studies on pulsatile and continuous flow during extracorporeal circulation (author's transl)]. 700 92

This study evaluated the effect of stimulating the central nervous system (CNS) with neostigmine, an inhibitor of acetylcholinesterase, on the blood lactate concentration in fed rats and in rats fasted for 48 hours. After the rat was anesthetized with pentobarbital, neostigmine was stereotaxically injected into the third cerebral ventricle. In fed rats, the central injection of neostigmine significantly increased the blood lactate level, while concomitantly increasing plasma glucagon, epinephrine and norepinephrine concentrations. Constant infusion of somatostatin throughout the experiments, to inhibit glucagon secretion from the pancreas, did not affect alterations in blood lactate by central injection of neostigmine. In adreno-medullated rats, CNS-stimulation by neostigmine still increased plasma norepinephrine significantly, however, the alteration in blood lactate was only one-third of that in intact rats. Intraperitoneal propranolol, but not phentolamine, prevented the rise in lactate. Neostigmine increased lactate in fasted rats as well as in fed rats. We conclude that in anesthetized rats, stimulation of the CNS by neostigmine increases blood lactate mainly through circulating epinephrine and partially through circulating norepinephrine or direct sympathetic nervous stimulation; glucagon does not appear to be involved in the increase in blood lactate.
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PMID:CNS regulation of blood lactate concentration in anesthetized rats. 791 Jun 51

In this study we examine the hypothesis that an inositol glycan phosphate can act similarly to insulin on intact cells. The inositol glycan phosphate used in this study (glycan alpha) was isolated previously from the glycoinositol phospholipid anchor of human erythrocyte acetylcholinesterase and was shown to have the structure glycine-ethanolamine-PO4-Man-Man-(N,N-dimethylethanolamine-PO4)Man- (N,N-dimethyl)GlcN-inositol-PO4. The cellular response investigated was the glucagon-stimulated activation of glycogen phosphorylase in rat hepatocytes. When hepatocytes were incubated with 20 nM glucagon for 4 min, the ratio of phosphorylase a activity to total phosphorylase increased from a basal value of 0.49 +/- 0.02 to 0.82 +/- 0.03 (mean +/- SE, n = 15). Inclusion of either 100 nM insulin or 3-10 microM glycan alpha during the glucagon incubation significantly decreased the glucagon-stimulated activity ratio to 0.74 +/- 0.03 for either agent. Furthermore, hepatocyte preparations differed in their response to insulin and were divided into insulin-responsive and -resistant groups. Glycan alpha had a significant effect only in the insulin-responsive group for which the observed activity ratio for 10 microM glycan alpha plus glucagon (0.68 +/- 0.05) compared closely with that for insulin plus glucagon (0.70 +/- 0.04). For the insulin-resistant group, the activity ratio in the presence of 10 microM glycan alpha was 0.81 +/- 0.03, unchanged from the control with glucagon alone. Because glycan alpha contains an inositol phosphate group, the effect of inositol cyclic 1,2-phosphate on the glucagon-stimulated activity ratio was determined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inositol glycan phosphate derived from human erythrocyte acetylcholinesterase glycolipid anchor and inositol cyclic 1,2-phosphate antagonize glucagon activation of glycogen phosphorylase. 834 43


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