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 induction of sodium pentobarbitone anaesthesia (45 mg/kg, ip) in 18 hour fasted mice produced a mild transient hyperglycaemia and a small but persistent increase in plasma glucagon concentrations. Plasma insulin concentrations became raised as the period of anaesthesia progressed. Plasma glucagon concentrations remained elevated as consciousness was regained, and a second episode of mile hyperglycaemia was observed at this time. Plasma free fatty acid concentrations were not altered by the anaesthesia and all parameters had returned to control values four hours after consciousness was regained. During anaesthesia glucose tolerance was impaired and the plasma insulin response to glucose and glucagon was enhanced. Higher plasma glucose and insulin concentrations were also observed after glucagon administration, and insulin hypoglycaemia tests revealed a decrease in the rate of glucose disappearance during anaesthesia. Four hours after consciousness was regained all these responses had returned to control values, except glucose tolerance which improved in comparison with controls. These results indicate that impaired glucose homeostasis during pentobarbitone anaesthesia is dependent on changes in both the secretion and physiological effects of insulin and glucagon.
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PMID:Insulin and glucagon during pentobarbitone anaesthesia. 699 5

The metabolic response to glucose infusion in anaesthetized normal and pancreatectomized dogs has been assessed. Normoglycaemia was achieved in the diabetic dogs with an external artificial B-cell which administered insulin into the peripheral circulation. No differences were found in the levels of blood glucose, glucagon, lactate, pyruvate and plasma non-esterified fatty acids, either in the fasting state or in response to glucose infusion. However, compared to normal animals normoglycaemic diabetic dogs had significantly elevated circulating levels of insulin and alanine at all times. Fasting levels of the same hormones and metabolites were also measured in conscious dogs. Blood pyruvate levels were higher, and plasma non-esterified fatty acid levels lower, in the anaesthetized animals. There were also minor but consistent changes in blood glucose and plasma insulin while glucagon, lactate and alanine levels were unaffected by anaesthesia. In conclusion, controlled barbiturate anaesthesia has relatively minor effects on the metabolic and hormonal status of the dog. The metabolic and hormonal response to glucose infusion in pancreatectomized dogs treated with an artificial B-cell was almost entirely normalized, except for peripheral hyperinsulinaemia and hyperalaninaemia.
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PMID:The metabolic and hormonal responses to glucose infusion in anaesthetized normal and diabetic dogs controlled by an artificial B-cell. 699 12

Synthetic bombesin (100 ng/min) was infused under pentobarbital anesthesia in normal dogs and in insulin deprived depancreatized dogs 4 days after surgery. The release of gut glucagon-like immunoreactive materials (gut GLI) calculated as the difference between the values measured using cross-reacting antiserum and a so-called pancreatic glucagon specific antiserum was markedly stimulated by bombesin infusion. Plasma glucagon immunoreactivity (GI) measured by pancreatic glucagon specific antiserum also showed a small increase, whereas plasma glucose decreased significantly with a transient rise in insulin. The plasma glucose level did not decrease in depancreatized dogs. Gut GLI response in the regional mesenteric vein to 5% glucose administered into the loop of the ileum was strongly augmented by bombesin infusion. It is concluded that (1) bombesin infusion decreased blood glucose level in normal dogs but not in depancreatized dogs. (2) Bombesin infusion markedly augmented the release of GLI from the intestine. (3) Bombesin also stimulated the release of glucagon which was probably of gastrointestinal origin. (4) Insulin release was stimulated transiently by bombesin infusion. Thus, a competition of gut GLI with glucagon at the glucagon receptor site may be an explanation of the reduction in blood glucose.
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PMID:Decrease in blood glucose and release of gut glucagon-like immunoreactive materials by bombesin infusion in the dog. 701 1

The significance of glucagon and of the sympatho-adrenal system for insulin secretion and hepatic glycogen depletion during exercise was studied. Male rats were either adrenodemedullated and chemically sympathectomized with 6-hydroxydopamine (SX) or sham-treated (C). During light ether anesthesia, cardiac blood for glucose analysis and a biopsy of the liver were obtained, and either antigen-stripped glucagon antibodies (A) or control gamma globulins (N) in saline were injected through the cardiac cannula. Subsequently, the rats swam in tepid water (33-34 degree C) for 100 minutes with a tail weight attached (2% of body weight). Then cardiac blood was drawn for analysis of glucose, insulin and glucagon, and a sample of the liver was collected. In both CA and CN rats, the blood glucose concentration tended to increase (p less than 0.1) during exercise, whereas hepatic glycogen depletion and the plasma insulin concentration were lower in CA rats compared to CN rats. In SX rats, the blood glucose concentration did not increase during exercise, and in SXA but not in SXN rats, the hepatic glucogen depletion was lower than in CN rats. The plasma insulin concentration was consistently higher in SX rats than in C rats, and was significantly decreased by glucagon antibodies in SX as well as in C rats. In conclusion, in exercising rats, glucagon enhances hepatic glycogen depletion. Furthermore, glucagon and the sympatho-adrenal system increase and decrease, respectively, the plasma insulin concentration.
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PMID:Significance of glucagon for insulin secretion and hepatic glycogenolysis during exercise in rats. 702 87

The effect of ventromedial (VMN) or basolateral (LHA) hypothalamic electrical stimulation on glucose and hormone production was examined in conscious and anesthetized male rats. Barbiturate treatment alone led to large increases of corticosterone and smaller but significant increases of glucose, insulin, and glucagon. When hypothalamic stimulation was combined with anesthesia, interactions between the hypothalamic sites and the awake-anesthetized conditions were observed. This was most evident with LHA placements, as awake rats exhibited mild hypoglycemia and hypoglucagonemia in response to low-level (approximately 10 microA rms) current, but no effects on these values were seen with VMN electrodes. With barbiturate anesthesia, the same level of stimulation led to severe hyperglycemia in both VMN and LHA rats and a mild hyperglucagonemia in the LHA group. No consistent effects of stimulation on immunoreactive insulin or corticosterone were detected at either hypothalamic site or in any anesthesia condition. The present results point out the important role anesthetics may play in studies defining functional aspects of the hypothalamus. Furthermore, our inability to elicit consistent autonomic responses with electrical stimulation, when compared with the effectiveness of both metabolic agents and pharmacologic stimuli, suggests that the sites integrating autonomic function may be diffusely distributed over the basal diencephalon.
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PMID:Glucose and endocrine responses to hypothalamic electrical stimulation in rats. 703 55

One hundred patients were studied prospectively to assess the incidence of spasm of the choledochoduodenal sphincter during biliary tract surgery performed under a fentanyl-supplemented anesthetic technique. The incidence of failure of passage of contrast medium into the duodenum was 3%. In each of the three patients with cholangiographic evidence of sphincter spasm, contrast medium flowed freely into the duodenum after the intravenous administration of 2 mg of glucagon. It is concluded that spasm of the choledochoduodenal sphincter is an uncommon occurrence during fentanyl-supplemented anesthesia and that this method of anesthesia is suitable for biliary tract surgery.
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PMID:Incidence of choledochoduodenal sphincter spasm during fentanyl-supplemented anesthesia. 719 6

Pheochromocytoma accounts for about 0.1 per cent of patients with diastolic hyperstension. It mimics many diseases varying from anxiety psychoneurosis to intracranial tumors. Cardinal symptoms include sevre headache (72 to 92 per cent), sweating (60 tp 70 per cent), palpitations (51 to 73 per cent), and hypertension (> 90 per cent) of which 50 per cent is sustained, 50 per cent paroxysmal. Many drugs (phenothiazines, Saralasin, antiemetics, steroids, etc.) have been reported as precipitating factors. Patients who should be screened for pheochromocytoma include: (1) all symptomatic patients with sustained or paroxysmal hyperstension; (2) asymptomatic hypertension; (3) all patients with MEA 2a,b (hyperparathyroidism, medullary carcinoma of the thyroid, neurocutaneous lesions) and their first degree relatives, even if the latter are asymptomatic and normotensive; (4) hypertension plus diabetes mellitis or hypermetabolism; (5) hypertensive episode during induction of anesthesia or radiologic procedure; and (6) hypertensive response during histamine administration, i.e., gastric analysis. Urinary metanephrine is the single best screening test. Plasma catecholamine determination is particularly helpful when collected before and immediately after an attack. Provacative agents (histamine, glucagon, tyramine) are needed rarely. Preoperative localization of the tumor can be done with nephrotomography IVP, computerized axial tomography, ultrasound, 131-I-19-iodocholesterol scan, arteriography, venography.
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PMID:Pheochromocytoma: clinical manifestations and diagnostic tests. 745 90

Glucagon has been proposed as the mediator of splanchnic hyperemia in portal hypertension. Employing an assay specific for pancreatic glucagon, we reevaluated the relationship between this peptide and portal hypertension in the portal vein (PV)-stenosed rat model addressing, in particular, the effects of anesthesia and surgical stress. Plasma glucagon levels were similar in sham-operated and portal hypertensive rats: glucagon, sham vs PV stenosed: 110.7 +/- 17.1 pmol/liter vs 140.6 +/- 23.3 pmol/liter (NS). Furthermore, plasma levels of glucagon and the related peptide VIP were not significantly influenced by anesthesia or surgical stress, and levels remained similar under all conditions in sham-operated and PV-stenosed animals. We conclude that pancreatic glucagon is not elevated in the PV-stenosed rat; differences between these results and those describing hyperglucagonemia in this model cannot be explained on the basis of a differential response to stress but may reflect differences in glucagon assay system.
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PMID:Glucagon, stress, and portal hypertension. Plasma glucagon levels and portal hypertension in relation to anesthesia and surgical stress. 764 85

The importance of glucagon on postoperative changes in hepatic amino-nitrogen conversion were investigated in six patients undergoing elective cholecystectomy for uncomplicated gall stones. Patients were given infusions of somatostatin (bolus of 6 micrograms/kg followed by continuous infusion of 6 micrograms/kg/h) from induction of anaesthesia to the end of investigation, the first postoperative day (30 hours). Controls were 16 patients undergoing the same procedures omitting the somatostatin infusion. In all patients blood concentration and plasma clearance of total alpha-amino-nitrogen, and amino acid stimulated rate of urea synthesis were measured. Elective cholecystectomy decreased blood alpha-amino-nitrogen concentration from mean (SEM) 2.9 (0.2) to 2.4 (0.1) mmol/l (p < 0.05), increased the clearance of total alpha-amino-nitrogen from 5.2 (0.3) to 6.6 (0.3) ml/s (p < 0.05), and increased the rate of amino acid stimulated urea synthesis from 27 (1) to 37 (2) mumol/s (p < 0.05) pointing to increased hepatic removal of amino-nitrogen at expense of plasma amino-nitrogen. Infusion of somatostatin prevented increase of glucagon for 24 hours after surgery, and prevented the negative changes in postoperative nitrogen homeostasis resulting from the postoperative changes in hepatic nitrogen conversion, suggesting glucagon as mediator. The exact mechanism remains in doubt, however, because of the multiple effects of somatostatin.
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PMID:Somatostatin prevents the postoperative increases in plasma amino acid clearance and urea synthesis after elective cholecystectomy. 779 29

Correlation between blood glucose, glucagon and adrenaline levels and gluconeogenesis was studied during the recovery from insulin-induced hypoglycemia in rats. Rats, overnight fasted, were intravenously injected with 40 microCi/kg of [U-14C]-lactate and 1 U/kg of porcine insulin under an anesthesia with pentobarbital sodium. Blood samples were drawn via the peripheral vein at 0, 5, 10 and 20 min. Plasma insulin level was 617 +/- 115 microU/ml at 5 min. Plasma glucose level was significantly decreased at 5 min (2.7 +/- 0.3 mM at 5 min v.s. 4.3 +/- 0.2 mM at 0 min, P < 0.01). Plasma glucagon and adrenaline did not significantly respond at 5 min, and then rised. Specific radioactivity of plasma [1-14C]-glucose was significantly higher at 5 and 10 min in the insulin-injected rat than the saline-injected rat (204 +/- 34 v.s. 130 +/- 14 d.p.m./mumol at 5 min, P < 0.01; 275 +/- 32 v.s. 186 +/- 16 d.p.m./mumol at 10 minm P < 0.01). These results suggest that lowering of blood glucose level stimulates gluconeogenesis independently of the release of counter-regulatory hormones in insulin-induced hypoglycemia.
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PMID:Insulin-induced hypoglycemia stimulates gluconeogenesis from 14C-lactate independently of glucagon and adrenaline releases in rats. 781 8


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