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)

Phenformin at high doses (10 mg/l, 50 mg/l, and 100 mg/l) increased the insulin and lactate output rates by the isolated perfused rat pancreas. Glucagon secretion was not modified. There was a statistically significant correlation between the increase in insulin and lactate output rates induced by phenformin. Intra-pancreatic L (+) lactate concentrations induced by phenformin were in the range of sodium L (+) lactate concentrations which experimentally stimulated insulin secretion by the same preparation. Thiamin pyrophosphate and sodium dichloroacetate, which promote the aerobic metabolism of pyruvate, opposed the phenoformin induced increase in lactate output by the isolated perfused rat pancreas and provoked as well a decrease in insulin release. These results suggest that the increase in insulin secretion following the administration of phenformin at high concentrations can be explained, to a large extent, by the increase in the production of lactate ions.
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PMID:Is lactate involved in phenformin-induced insulin secretion? 43 87

Polypeptide material displaying glucagon-like immunoreactivity was isolated from porcine colon using immunoaffinity chromatography. The immunoreactive material was tightly bound to high molecular weight proteins but was dissociated by 0.1% w/v sodium dodecyl sulphate solution into immunoreactive components of approximate molecular weights 12,000,8000,5000 and 3000. These components reacted at least 50 times more strongly with antibodies specific for the N-terminal region of glucagon than with antibodies specific for the C-terminal region of glucagon. While the 8000 and 3000 dalton fractions were homogeneous, the 12,000 and 5000 dalton fractions were resolved into multiple bands by isoelectric focusing. The 12,000 dalton fraction was devoid of glycogenolytic and lipolytic activity, was not insulin releasing and showed no ability to bind to receptor sites specific for glucagon on hepatic plasma membranes and to active hepatic adenylate cyclase. The 8000 and 5000 dalton components showed weak lipolytic activity. The possible significance of colonic glucagon-like immunoreactivity relative to pancreatic glucagon and immunoreactivity from other tissues is discussed.
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PMID:Physicochemical and biological properties of glucagon-like polypeptides from porcine colon. 45 44

Glucagon was infused through the porta or through the left renal artery in dogs. Another group of dogs were infused with glomerulopressin through the left renal artery. It was observed that glucagon when infused through the portal vein enhanced the glomerulopressin production and the glomerular filtration rate (GFR). When glucagon was infused intrarenally it did not alter GRF but it had a direct tubular action decreasing sodium reabsorption in the proximal tubule. Glomerulopressin infused intrarenally increased GRF and potassium excretion. The results suggest that the increase in GFR was due to increase in glomerulopressin activity. There are three reasons for this statement: a) GRF increased when glomerulopressin activity was high, but not when there was a low activity, 5) intrarenally infused glomerulopressin produced a very significant change in the GFR of the infused kidney, while the GRF of the contralateral kidney remained unchanged and c) intrarenally administered glucagon had no effect on GFR.
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PMID:Effect of glucagon and glomerulopressin on the renal function of the dog. 45 30

Serum-free media containing 10-50 ng insulin, glucagon and epidermal growth factor (EGF) ml-1 stimulate adult rat hepatocyte proliferation in 10-15 day old primary liver cell cultures. The kinetics of this response simulate hepatocellular transitions that accompnay liver regeneration after 67% hepatectomy. Amiloride, a Na+ influx inhibitor, reversibly blocks these transitions in vitro (ID50 approximately 0.02 mM) and in vivo (ID50 approximately 25 mg kg-1). Inhibition is observed with other cation flux modulators, including ouabain (ID50 approximately 0.2 mM), 0.2 microM monensin and 0.2 microM nigericin, but not with 0.3 mM furosemide or tetrodotoxin. The prereplicative interval in culture (0-12 hr) is characterized by preferential cellular responsiveness to EGF (0-3 hr) followed by insulin plus glucagon (3-12 hr). Parallel culture and animal studies show that the amiloride-sensitive and prereplicative intervals coincide. In culture, a "burst" of 22Na+ influx, stimulated by peptide-supplemented media within 1 min but decreased later at 12 hr, is retarded by amiloride. This drug also blocks delayed prereplicative events involving increased amino acid "A" transport system function at 4-8 hr, and 3H-uridine and 3H-leucine incorporation into RNA and protein, respectively, at 8-12 hr. These findings suggest that at least two time-ordered processes are necessary to initiate hepatic growth fully: first, activation of Na+ flux systems by peptides similar or identical to EGF; and second, potentiation of these and subsequent cellular events by the combined action of insulin plus glucagon. [Amiloride: N-amidino-3,5-diamino-6-chloropyrazinecarboxamide; furosemide: 4-chloro-N-furfuryl-5-sulfamoylanthranilic acid; AIB: alpha-aminoisobutyric acid; ID50: administered dose giving 50% inhibition of a maximal response; dFBS: dialyzed fetal bovine serum; L.I.: 3H-dT nuclear labeling index.]
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PMID:Increased sodium ion influx is necessary to initiate rat hepatocyte proliferation. 50 19

The possibility that gastrointestinal hormones influence biliary lipid secretion was studied further in chronic bile fistula dogs and subsequently in a patient with a balloon-occludable t-tube. After stabilization of bile flow in the dog by infusing 500 mg/hr sodium taurocholate, glucagon and insulin increased bile flow, decreased cholesterol output, and had no effect on phospholipid or bile salt output. Similarly, during reinfusion of bile in the human subject, glucagon increased bile flow, decreased cholesterol output and had no effect on bile salt output. Phospholipid secretion decreased, as had occurred at a lower bile salt infusion rate in the chronic bile fistula dog. These findings suggest that glucagon or insulin may play a role in regulating cholesterol secretion in dog and man, and that mechanisms other than simple dilution of micelles are operative.
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PMID:Glucagon or insulin suppressed biliary lipid excretion in dog and man. 51 71

Glucagon (90 to 880 pg.ml-1) failed to influence electrical activity or fluxes of sodium and chloride across human jejunal and ileal mucosa in vitro. These results suggest that the intestinal secretion and diarrhoea produced in vivo in man during intravenous infusion of glucagon may be produced by changes in motility and blood flow and not directly by activating an ion secretory mechanism as is the case in cholera.
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PMID:Failure of glucagon to influence ion transport across human jejunal and ileal mucosa in vitro. 60 34

The effects of glucagon administration through intracerebroventricular (ICV), third ventricular (TV) and intracisternal (I") routes on urinary sodium and potassium concentration have been studied in mongrel dogs. The central administration of glucagon resulted in a significant decrease in urinary sodium concentration (P less than 0.01) and increase in urinary potassium concentration (P less than 0.001). This change in urinary sodium and potassium concentration on central administration of glucagon was abolished in animals which were ventured to either sympathetic denervation or adrenalectomy. The observations in the present study suggest that the changes in urinary sodium and potassium concentration on central administration of glucagon, are due to increased secretion of some substance from the adrenals and the probable efferents might be the sympathetic fibres.
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PMID:Effect of centrally administered glucagon on urinary sodium and potassium concentration in dogs. 61 85

Rat hepatic pyruvate kinase (type L) has been purified to homogeneity by a simple, rapid procedure involving DEAE-cellulose chromatography and elution from a blue Sepharose column. The enzyme was homogeneous by the criteria of sodium dodecyl sulfate disc gel electrophoresis, had a subunit molecular weight of 57,000, and a specific activity of 558 units/mg of protein at 30 degrees. In order to test whether the enzyme is phosphorylated in vivo, rats were injected with radioactive inorganic phosphate. Incorporation into pyruvate kinase was determined after purification of the enzyme to homogeneity as well as after specific immunoprecipitation of the enzyme from partially purified preparations. Sodium dodecyl sulfate disc gel electrophoresis revealed that 32P was incorporated into the enzyme in both cases. Glucagon administration in vivo resulted in a 200 to 300% increase in the incorporation of 32P into the enzyme which was correlated with an inhibition of enzyme activity and an elevation of hepatic levels of cyclic AMP. These results represent the first demonstration of in vivo phosphorylation of a hepatic glycolytic enzyme and strongly support the hypothesis that glucagon regulates pyruvate kinase activity, at least in part, by a phosphorylation mechanism.
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PMID:Stimulation of glucagon of in vivo phosphorylation of rat hepatic pyruvate kinase. 62 Nov 97

To examine the role of basal insulin and glucagon secretion in potassium and sodium homeostasis, somatostatin, a potent inhibitor of insulin and glucagon secretion, was infused for 5 h into healthy human subjects, maturity-onset diabetes, juvenile-onset diabetics, and normal dogs. Infusion of somatostatin resulted in an increase in serum potassium (0.5-0.6 meq/liter) in normal subjects and maturity-onset diabetics, but not in juvenile-onset diabetics despite equivalent reductions in plasma glucagon in all three groups. A similar rise in serum potassium was observed in normal conscious dogs given somatostatin and was reversed by insulin replacement. Urinary excretion of potassium was unaffected by somatostatin. In dogs given intravenous potassium chloride in doses (0.375 meq/kg per h) which do not alter basal insulin levels, the rise in serum potassium (0.6 meq/liter in controls) increased 100% when somatostatin was administered together with the KCl infusion. Addition of replacement doses of insulin to the somatostatin infusion resulted in increments in serum potassium which were comparable to infusion of KCl alone. Urinary potassium excretion rose after KCl administration and was unchanged by the addition of somatostatin. Serum sodium concentration was unaffected by somatostatin administration in both the human and dog studies. However, urinary sodium excretion displayed a biphasic response falling by 20-60% within the first 2 h of somatostatin administration and then rising to values 50-80% above basal levels at 3-4 h. Inulin and p-aminohippurate clearances were unaffected by somatostatin. It is concluded that (a) potassium homeostasis is influenced by basal insulin levels in the absence of which serum potassium concentration rises and potassium tolerance declines; (b) this effect of insulin is mediated via extrarenal mechanisms of potassium disposal; (c) somatostatin has a biphasic effect on urinary sodium secretion, the mechanism of which remains to be established.
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PMID:Influence of basal insulin and glucagon secretion on potassium and sodium metabolism. Studies with somatostatin in normal dogs and in normal and diabetic human beings. 62 Dec 84

Treatment with glucagon in addition to blood transfusion was compared with blood transfusion alone after one hour of hemorrhagic shock in the rat. In liver tissue Na+ increased and K+ decreased during haemorrhagic shock. After treatment the initial values were restored equally in both groups within ten minutes. Incubation of liver slices in cold Krebs' solution resulted in a pronounced increase in Na+ and decrease in K+, the values being partially restored to initial levels after subsequent incubation at 37 degrees. Thirty minutes after treatment the liver slices obtained from rats given glucagon showed a more normal ion composition after leaching and rewarming than slices from rats not given glucagon. ATP decreased and glucose and lactate increased in liver tissue during hemorrhagic shock. These variables were partially restored 30 minutes after treatment. No difference between the treatment groups was noted. Animals trreated with glucagon were, however, more efficient in reducing the elevated blood lactate level. The results suggest that the use of glucagon in the treatment of hemorrhagic shock might be of benefit for cellular function in the liver.
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PMID:Effect of glucagon and blood transfusion on liver metabolism in hemorrhagic shock. 62 13


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