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 isolated perfused rat pancreas was used to investigate the effect of oleic acid on glucagon secretion in response to 10 mmol/l arginine. In the absence of oleic acid and at 2.5 mmol/l calcium, arginine induced a biphasic glucagon secretion. At lower extracellular calcium concentration (1.0 mmol/l), the second phase of glucagon release was reduced, the first phase being unchanged. In the presence of 1,500 mumol/l oleic acid, the glucagon response to arginine was also biphasic, but second phase release was markedly inhibited, the first phase glucagon release being unchanged. Such an effect was not obtained when oleic acid concentration in the medium was 750 mumol/l. These results demonstrate that high concentrations of oleic acid inhibit glucagon secretion in response to arginine from the isolated perfused rat pancreas and support the concept that circulating free fatty acid levels are involved in the control of glucagon secretion.
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PMID:Effect of oleic acid on arginine-induced glucagon secretion by the isolated perfused rat pancreas. 55 Jun 71

Glucagon and the pancreatic homogenate preparations to be tested for hypocalcemic effects were injected either intravenously or intraperitoneally in thyroparathyroid intact dogs and in dogs after thyroparathyroidectomy, respectively. Evidence has been presented that, in thyroparathyroid intact dogs, pancreatic tissue homogenate and the residue of such homogenate demonstrated a maximal hypocalcemic effect and that, in the thyroparathyroid intact dog, glucagon produced a hypocalcemic effect but did not produce a significant effect on dogs after acute thyroparathyroidectomy. On the other hand, the hypocalcemic effect of residue was equally effective both in dogs after thyroparathyroidectomy and in thyroparathyroid intact dogs; there was evidence that intravenous infusion of the residue resulted in a more rapid decrease in serum calcium levels compared with the intraperitoneal infusion after thyroparathyroidectomy of dogs being maintained four to five days with parathormone. Although final conclusions are not justifiable, the results suggest that a pancreatic factor other than glucagon has hypocalcemic effects and might explain the hypocalcemia observed during acute pancreatitis.
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PMID:The hypocalcemic activity of pancreatic tissue homogenate in the dog. 55 40

The effect of Verapamil, a potent calcium antagonist, upon pancreatic glucagon release was investigated in the isolated, perfused canine pancreas. Verapamil at concentrations ranging between 10(-5)-10(-4) mol/l caused a dose-related inhibition of glucagon release at a glucose concentration of 25 mg/dl. The inhibition was an immediate and reversible phenomenon. The inhibitory effect was reduced when the Ca2+ concentration was increased from 1.3 to 5.0 mmol/l. The results are compatible with earlier findings from our laboratory demonstrating that calcium plays a key role in the stimulus-secretion coupling of glucagon release.
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PMID:Effect of Verapamil on pancreatic glucagon release from the isolated, perfused canine pancreas. 61 40

Intravenous application of 1 mg glucagon causes a significant decrease of the magnesium, calcium, and phosphate concentrations in the serum. Concerning the potassium level there is a biphasic change of concentration. Initially a significant increase of the potassium concentration is to be measured which transgresses into a longer phase of decrease of concentration. The possible causes of these changes of electrolytes after application of glucagon are discussed and it is referred to the possible clinical importance. In longer therapeutic application of glucagon a control of the serum parameters of the electrolytes metabolism appears indicated.
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PMID:[The effect of glucagon on serum electrolyte concentrations in man]. 64 44

The temperature optimum for the positive inotropic response of guinea-pig isolated atria to single submaximal doses of isoprenaline was 25 degrees C. This was well separated from that for rate responses (37.5 degrees C). This separation was not due to changes in catechol-0-methyl-transferase or phosphodiesterase activity since it occurred with orciprenaline alone and in the presence of theophylline. The rate optima for aminophylline, histamine, glucagon, ouabain, calcium chloride and dibutyryl cAMP were essentially the same as for isoprenaline. The temperature-dependences therefore lie at a common ultimate pathway leading to the rate response. The site of temperature-dependence of the inotropic response to isoprenaline is not at the common contractile mechanisms since its optimum differed from those of ouabain and CaCl2. Activity of cAMP and its production were also eliminated as possible sites from differing optima of aminophylline, histamine and dibutyryl cAMP. The temperature-dependence may lie at the beta-adrenoceptor itself, possibly adenyl cyclase. This may be shared by glucagon although tachyphaylaxis made its optimum difficult to determine.
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PMID:Possible sites of temperature-dependent changes in sensitivity of the positive inotropic and chronotropic responses to sympathomimetic amines by comparisons of the temperature optima for a range of agonists. 64 19

Pancreatitis was induced in 11 miniature pigs by infusing a bile salt-trypsin solution into the pancreatic duct. Seven animals served as sham-operated controls. Serum ionized calcium, total calcium, albumin, total protein, inorganic phosphorus, urea nitrogen, magnesium, insulin, glucagon, and hematocrit were determined every six to 12 h over a period of one week in both test and control animals. We observed significant decreases in ionized and total calcium, modest decreases in albumin, and significant increases in the inorganic phosphorus, urea nitrogen, and hematocrit in the pancreatitic pigs. The latter two findings were consistent with early acute hypovolemia. Glucagon and insulin appeared to play no role in the hypocalcemia. Glucagon concentrations increased to the same degree in both test and control animals, probably as a result of the stress of being handled and operated on. The highest concentrations of inorganic phosphorus and the lowest concentrations of both ionized and total calcium were seen 18 h after the induction of pancreatitis in the test animals. These findings suggest that parathyrin (parathormone) was not being secreted in adequate amounts, or that the target organs were unresponsive to parathyrin.
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PMID:Biochemical changes in a porcine model of acute pancreatitis. 65 76

At concentrations below 50 micronM, phenethylbiguanide enhanced the initial rate of enertized Ca2+ uptake into energized guinea pig liver mitochondria by as much as 45 per cent; Ca2+-stimulated O2 uptake increased in parallel. The biguanide concentration that enhanced Ca2+ uptake maximally was at least 15 times lower than that required for 50 per cent inhibition of respiration. Kinetic studies indicated that the enhanced rate of Ca2+ transport resulted from an increase in Vmax, while Km for Ca2+ was unaffected by the biguanide. Several other organic cations known to lower blood sugar in intact animals or to block the hepatic gluconeogenic response to glucagon also enhanced the mitochondrial Ca2+ uptake rate; three of these compounds did not inhibit respiration even at high concentrations. One organic cation, triethyltin, which is a potent respiratory inhibitor that does not affect blood sugar, had no effect on Ca2+ uptake. We concluded that enhancement of the mitochondrial Ca2+ uptake rate is related to the mechanism of therapeutic blood sugar lowering by these drugs, probably by impairing the gluconeogenic response of the liver to glucagon.
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PMID:Enhancement of the mitochondrial Ca2+ uptake rate by phenethylbiguanide and other organic cations with hypoglycemic activity. 65 23

The effect of extracellular calcium concentration on the insulin and glucagon release in response to arginine from the isolated perfused rat pancreas, has been studied. All the experiments were carried out in the absence of glucose in the perfusate. Arginine 10 mM elicited a biphasic glucagon release, and a monophasic insulin response. In the presence of calcium 2.5 mM an increase of total insulin and glucagon in response to arginine were obtained. The increase in glucagon release was only detectable during the second phase, while first phase was not modified by the concentration of calcium present in the perfusate. The results of this study show that extracellular calcium concentration influences positively insulin and glucagon responses to arginine in vitro.
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PMID:Effect of various concentrations of calcium on arginine-induced insulin and glucagon release in vitro. 69 8

The role of calcium transport into the pancreatic A2-cell in release of glucagon was studied in the perfused in vitro rat pancreas exposed to the organic calcium-antagonist verapamil (10 and 20 microns). As judged by the inhibitory effect of verapamil, a sufficient influx of calcium was required for glucagon release to be stimulated by either arginine (10 mM) or a lowering of the glucose concentration from 16.6 to 3.3 mM. However, such was not the case for glucose to inhibit the release of glucagon or when the A-2-cell was established in a stimulated state during prolonged exposure to a low, 3.3 mM, glucose concentration. These findings suggest that the role of inwardly directed transport of calcium in the secretory process of the A2-cell is of a complex nature, being dependent on the type of stimulus employed (arginine or glucose) and, in the case of glucose, on the static or dynamic state of the cell. The intimate mechanisms by which calcium exerts such complex effects on the secretory process in the A2-cell remain to be elucidated.
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PMID:The role of calcium in glucagon release. Studies with verapamil. 70 Feb 62

The effect of haloperidol, a dopaminergic antagonist, on insulin and glucagon secretion was investigated using the isolated, perfused canine pancreas. Haloperidol at 4 X 10(-7) to 10(-5) mol/l caused a dose-dependent inhibition of glucagon release both at low (25 mg/100 ml) and high glucose concentrations (150 mg/100 ml). At the low glucose concentration insulin release was already maximally suppressed. At the high glucose concentration haloperidol (4 X 10(-7) to 10(-5) mol/1) also caused a dose-dependent inhibition of insulin release. Haloperidol (10(-5) mol/1) inhibited dramatically pancreatic A and B cell responses to isoproterenol (2 ng/ml), acetylcholine (1 mumol/1) and arginine (5 mmol/1). The inhibitory effect of haloperidol on both glucagon and insulin release could be eliminated by increasing perfusate calcium concentration from 1.3 to 8.8 mmol/1. These findings suggested that haloperidol blocks glucagon and insulin release in a somatostatin-like manner by affecting a fundamental step of the stimulus-secretion coupling, probably by interfering with calcium handling of the pancreatic A and B cells.
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PMID:Haloperidol, a dopaminergic antagonist: somatostatin-like inhibition of glucagon and insulin release from the isolated, perfused canine pancreas. 71 Jul 56


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