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 treatment of acute pancreatitis as currently practised in Austria was evaluated by means of a questionnaire mailed to all medical and surgical departments in Austrian hospitals. Fasting, analgesics and parenteral fluid therapy are applied routinely and proteinase inhibitors are used in nearly all hospitals. The efficacy of placing the pancreas at rest by withdrawal of oral fluids, nasogastric suction or antacids is variably assessed. Pharmacological inhibition of pancreatic secretion is achieved mainly by anticholinergics, whilst less often glucagon is prescribed. Antibiotic prophylaxis is widely applied. The main indications for surgery are complications and pre-existing biliary tract disease. These results are compared with the literature.
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PMID:[The treatment of acute pancreatitis in Austria: results of a questionnaire]. 39 Aug 91

Sixty-two cases of acute pancreatitis, evaluated for severity according to uniform standards, were treated identically except that patients in one group received glucagon hydrochloride (group A) and those in the other oxyphenonium bromomethylate (group B). Each of the two homologous series comprise 31 patients, and mortality was the same for both groups (3/31, 10%). Statistical comparison of both series showed no significant differences in frequency of expected complications nor in fall of serum amylase levels. During treatment, serum calcium levels were significantly reduced in group A (P less than .005), and the duration of the abdominal pain was shortened (P less than .05). The volume of gastric aspirate was smaller in group B (P less than .005), and vesical catheterization proved necessary more frequently (P less than .005). Thus, similar results are obtained when glucagon or anticholinergics are employed in the treatment of acute pancreatitis, although secondary effects differ.
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PMID:Glucagon vs anticholinergics in the treatment of acute pancreatitis. A double-blind controlled trial. 41 63

Personal experience in the treatment of acute pancreatitis with glucagon is reported. Results are highly satisfactory and encouraging in oedematous, interstitial and circumscribed steatonecrotic forms, disappointing where the disease has caused extensive damage to the gland.
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PMID:[Treatment of acute pancreatitis with glucagon]. 47 Dec 77

The inhibitory action of both calcitonin (CT) and glucagon (GK) on human pancreatic secretion has been evaluated in detail. The reduction of enzyme secretion expressed as percentage corresponded to 60--80% of the initial values in response to both CT and GK when the hormones were given as single infusions during background stimulation with secretin or with secretin plus cholecystokinin-pancreozymin (CCK-PZ). After withdrawal of GK-infusion the return to normal values of enzyme secretion was distinctly faster than after CT, thus reflecting a more rapid degradation of circulating GK than of CT. In the presence of stimulation with secretin plus CCK-PZ, the combined administration of CT and GK did not enhance the inhibitory actions of CT and GK. Fluid and bicarbonate secretions were not affected by either CT or GK. The results suggest that CT and GK inhibit human pancreatic enzyme secretion by similar modes of action. Therefore, the combined administration of both CT and GK does not offer a reasonable approach to the treatment of acute pancreatitis.
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PMID:Similar modes of action of calcitonin and glucagon in inhibiting pancreatic enzyme secretion in man. 54

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

Metabolic studies of a 9-year-old girl with primary type V hyperlipoproteinemia demonstrated normal glucose tolerance, plasma insulin and glucagon responses to stimuli, and serum uric acid level. Fasting plasma triglyceride levels rapidly increased when the patient received a diet containing 40% of the total calories as fat and rapidly decreased on a 10% fat diet. Hepatic and nonhepatic lipase activities in postheparin plasma were normal, thus excluding type I hyperlipoproteinemia. Because of the potential complication of acute pancreatitis in this disorder, early diagnosis and prompt institution of diet therapy is important.
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PMID:Primary type V hyperlipoproteinemia in childhood. 57 87

Acute pancreatitis was induced in 245 rats by retrograde instillation of Na-taurocholate into the pancreatic duct. Mortality rate in animals treated 6-hourly with glucagon (1 mg/kg) after induction of pancreatitis was 50% as compared to 30% deaths in the controls treated with 0,9% NaCl (chi2-test: p less than 0,05). Mortality rate in animals treated 6-hourly with the same dose of glucagon before induction of pancreatitis was 36,5% as compared to 28% deaths in the corresponding controls (chi2-test: p greater than 0,05). Glucagon in lower doses (0,1-0,5 mg/kg every 6 hours) did not alter mortality rates as compared to animals treated with 0,9% NaCl. 2. A nonletal form of pancreatitis was induced in 26 rats by ligation of the pancreatic duct. Injection of glucagon (1 mg/kg) seemed to suppress amylase activities in blood for a short period of appr. 1 hour. However, 7 and 9 hours after induction of pancreatitis, amylase activities were significantly higher in animals treated one or two times with glucagon as compared to untreated controls. It is concluded that glucagon in the high dose of 1-4 mg/kg/24 hours does not only not influence the course of acute experimental pancreatitis in rats but can even deteriorate it.
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PMID:A controlled trial of glucagon in acute experimental pancreatitis in rats. 60 26

The amylase/creatinine clearance ratio (Cam/Ccr ratio) was determined in 239 subjects. In 87 hospitalised patients without pancreatic disease (controls) the Cam/Ccr ratio was 3.02 +/- 0.69 (mean +/- ISD). The ratio was above the normal range in all patients with acute pancreatitis but was normal in those with chronic pancreatitis and carcinoma of the pancreas. In 18 patients with choledocholithiasis a raised ratio distinguished those with pancreatitis as assessed independently by the surgeon at laparotomy from those with a macroscopically normal pancreas. Raised Cam/Ccr ratios were also found in diabetics with ketoacidosis and in three patients with fulminant alcoholic liver disease. Though a positive correlation was found between the Cam/Ccr ratio and serum creatinine concentration, abnormally high ratios did not occur in 30 patients with chronic renal failure. A significant increase in Cam/Ccr ratios was produced in six healthy volunteers by intravenous injection of glucagon. However, it is unlikely that hyperglucagonaemia alone accounts for the increased Cam/Ccr ratio seen in acute pancreatitis, as no correlation was found between the clearance ratio and the plasma glucagon concentration in a series of patients. In two other patients in whom excess circulating pancreatic polypeptide was detected the Cam/Ccr ratio was normal. It is concluded that, in view of the sensitivity and relative specificity of finding an increased Cam/Ccr ratio in acute pancreatitis, its determination should be valuable clinically, especially in those cases of hyperamylasaemia where the cause is in doubt. The mechanism whereby the ratio is increased is unknown, and it is unlikely that either glucagon or pancreatic polypeptide is a major factor in its production.
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PMID:Mechanism and specificity of increased amylase/creatinine clearance ratio in pancreatitis. 60 90

Differences in metabolic homeostasis in 12 patients with initial vs. eight patients with repeated attacks of acute pancreatitis have been compared during the acute phase of the disease. As a group, subjects with a previous history of pancreatitis had significantly lower glucagon concentrations (P less than 0.002) for the over all 24-hour study period. Conversely, the serum concentrations of blood sugar, insulin, growth hormone, gastrin, cortisol, nonesterified fatty acids, triglycerides and cholesterol failed to distinguish between the two patient groups. Likewise, immunoreactive plasma parathyroid hormone and calcitonin levels were comparable in both patient populations. Of the measurements considered, it would appear therefore that plasma immunoreactive glucagon is the best indicator of previous pancreatic inflammation. Evaluation of parenchymal integrity during an episode of acute pancreatitis would be of prognostic and therapeutic value in this disease.
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PMID:First 24 hours of acute pancreatitis. A biochemical and endocrine evaluation of initial versus repeated attacks. 69 15

Glucagon is secreted not only by A2-cells of the pancreatic islets but also by A cells in the gastric fundus and duodenum. Several reports have demonstrated that the glucagon plasma concentration is increased in genetic diabetes as well as in many conditions associated with a decreased glucose tolerance such as hepatic cirrhosis, myocardial infarction, infectious diseases, burns, taumatic shock, glucagonomas, acute pancreatitis, acromegaly, pheochromacytoma and Cushing's syndrome. Hyperglucagonemia is particularly important in diabetic ketoacidosis and in non-ketotic hyperosmolar coma. The mechanisms responsible for the diabetic's hyperglucagonemia remain controversial. According to several authors, the increased glucagon secretion is, for its main part, secondary to a prolonged defect in insulin secretion and thus relatively insensitive to an acute insulin administration. According to others, the A cell abnormality is of primary origin, independant from insulin deficiency and its effects are cumulative with those of the insulin lack. Several reports dealing with induced or spontaneous experimental diabetes are in favor of the first or the second hypothesis. It appears likely that glucagon plays a role in the metabolic derangments of diabetes. Indeed, hepatic glucose production is closely related to the ratio of molar concentrations of insulin and glucagon. Finally, in insulin-dependant diabetics, somatostatin infusion reduces plasma glucagon concentration and blood glucose and prevents the development of ketosis after withdrawal of insulin therapy. These results illustrate the contribution of glucagon in the pathogenesis of hyperglycemia and ketosis. Several arguments have been accumulated in favor of the following concept: diabetes hyperglycemia results both from glucose under-utilization secondary to insulin lack and from hepatic glucose over-production due to glucagon excess. Although controversial, the role of glucagon in ketogenesis appears likely.
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PMID:[The role of glucagon in hyperglycemia. A review (author's transl)]. 79 28


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