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 influence of glucagon and aprotinin ('Trasylol') on the death-rate of acute pancreatitis has been studied in a randomised double-blind multicentre trial. The death-rate in 257 patients was 11%. In the doses used neither drug was found to diminish the risk of death.
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PMID:Death from acute pancreatitis. M.R.C. multicentre trial of glucagon and aprotinin. 7 49

A questionnaire on the conservative treatment of acute pancreatitis was answered by 312 surgical [n = 139] and medical [n = 173] departments from all over Western Germany and from West-Berlin. Nearly total positive agreement was found about routine administration of parenteral fluids and on the prohibition of oral food and fluids. The application of glucocorticoids, glucagon, heparin in small doses and of a carboanhydrase inhibitor [Diamox] is rejected by most of the departments. Renal failure is treated in 63% by hemodialysis and in 37% by peritoneal dialysis. There is great disagreement between the answers about the administration of atropine, antacids and aprotinin [Trasylol]. Antibiotics are applied routinely by 63% of the surgical and 70% of the medical departments.
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PMID:[The conservative treatment of acute pancreatitis in the Federal Republic of Germany in 1977 (author's transl)]. 10 62

Severe resistance to subcutaneous insulin but sensitivity to intravenous insulin persisted for 15 months in a 17-year-old diabetic girl. Heat-labile insulin-degrading activity was present in the patient's ketotic sera and in the 100,000 g fraction (soluble fraction) of adipose tissue. Serum-degrading activity was not inhibited by N-ethylmaleimide. The soluble fraction also degraded glucagon and B chain but not growth hormone or myoglobin. It was inhibited by incubation with the patient's nonketotic sera, normal sera, or Trasylol. Glutathione-insulin-transhydrogenase (GIT) activity was 66% of normal. The biopsy of adipose tissue at remission showed a normal level of insulin- and glucagon-degrading activity. The activity was eluted from Sephadex G200 as a single peak and had properties consistent with those of the insulin-specific protease (ISP). The increased degrading activity present during insulin resistance had properties not shared with ISP, suggesting the presence of an uncharacterized protease.
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PMID:Insulin resistance caused by massive degradation of subcutaneous insulin. 10 40

Acute pancreatitis may present as the mild edematous type or the more rare and dangerous hemorrhagic form. The effects of the latter are believed to be due to the activation of pancreatic enzymes, notably trypsin. Therefore attempts are being directed towards suppression of pancreatic enzyme activation in the management of the condition. Aprotinin and glucagon are the agents for this purpose that have received most attention. Patients with acute hemorrhagic pancreatitis are subject to respiratory failure, which is not detectable early by clinical evidence, so that early monitoring of pulmonary function by the determination of arterial blood-gas pressures is desirable. This is borne out by the findings in six fatal cases.
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PMID:Symposium on pancreatitis: 1. Conservative management of acute pancreatitis. 30 73

The unpredictable course of acute pancreatitis needs a careful surveyance of the patient in the first days of the acute attack in order to apply therapeutic measures adequate to the severity of the symptoms. The avoidance of food or drink and gastric suction appears to be sufficient to prevent endogenous stimulation of the gland while there is probably no benefit of anticholinergic drugs or carboanhydrase inhibitors. Early adequate substitution of fluids using watery solutions, plasmaexpanders or blood is of decisive importance. For treatment of pains spasmoanalgetics, synthetic opium derivatives or infusion of procain are recommended. Tetracyclines should be given to prevent secondary infections. Trasylol is indicated only, if the benefit of the drug just now proven in one therapeutical trial will be confirmed in another study. The effectiveness of glucagon or calcitonin has not yet been proven. The medical treatment "by all means" is being replaced by elective surgical measures. After recovery etiological factors have to be determined by a number of routine investigations in order to prevent recurrency of the disease.
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PMID:[Therapy of acute pancreatitis]. 82 86

All 78 patients with acute pancreatitis admitted to one hospital in a 2-year period were included in a prospective survey of conservative management. The overall mortality rate was 11.5 per cent, being 46 per cent for 11 patients subjected to early laparotomy and only 6 per cent for patients managed without operation. Twenty-six patients were considered to have severe acute pancreatitis and all 9 deaths occurred in this group. Biliary disease was present in 51 per cent of patients, and the majority of those with biliary disease were over 60 years old. Alcohol-related acute pancreatitis occurred in 26 per cent of the total patients, and none of this group was over 60 years old. Acute pancreatitis was considered idiopathic in origin in only 13 per cent of the patients. Elective biliary surgery in 30 patients resulted in freedom from recurrent attacks of acute pancreatitis for the follow-up period (12-30 months). The results compare favourably with those in which glucagon and high dosage aprotinin (Trasylol) have been utilized in the management of acute pancreatitis.
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PMID:A prospective study of acute pancreatitis. 108 65

Seventy patients admitted to Waikato Hospital between 1964-74 with acute pancreatitis have been reviewed. Biliary tract disease and alcohol are the most common aetiological agents. The disease is most common in middle age. Europeans and Polynesians have similar incidence rates. The diagnosis is frequently not made at admission and most admissions are in the afternoon or early evening. Radiology is helpful in the diagnosis although nonspecific. Abnormal biochemistry is discussed and related to mortality. Additional tests, serum catalase/methaemalbumin are promoted to assist in the diagnosis and indicating the severity of the disease. Glucagon and Trasylol are discussed as being beneficial in this disease and combination therapy is suggested. The role of surgery is discussed.
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PMID:Acute pancreatitis ten years experience in the Waikato district. 108 Dec 8

We have studied insulin degrading activity (IDA) in cultured human fibroblasts and assessed the effect of various inhibitors of insulin processing on IDA. To evaluate the role of three enzymes of insulin degradation (neutral protease, microsomal glutathione insulin transhydrogenase, and lysosomal acid protease), we subfractionated homogenized fibroblasts into membrane (and nuclei) cytosol, mitochondria, microsomes, and lysosomes. Greater than 90% of IDA was found to be present in the cytosolar fraction containing neutral protease. IDA in intact fibroblasts was completely inhibited by 1 mM N-ethylmaleimide and partially by 0.5 mM dansylcadaverine (75%), 0.5 mM chloroquine (48%), 1 mg/ml bacitracin (32%) and Trasylol (30%). Lidocaine (5 mM) and glucagon (10(-6)M) exhibited about 15% inhibition with minimal inhibition (7%) by nonsuppressible insulin-like activity. Study of similar inhibitors on subfractionated components indicated inhibition of cytosolar enzyme by N-ethylmaleimide (100%), glucagon (30%), chloroquine (41%), nonsuppressible insulin-like activity (30%), Lidocaine (25%), dansylcadaverine (16%), and bacitracin (11%). Incubation of ammonium sulfate-fractionated cytosolar enzyme at 37 C with A14-125I-insulin resulted in generation of two intermediate peaks as early as 1 min. These peaks could be identified by HPLC but not by molecular sieve chromatography. These intermediates exhibited less immunoprecipitability with antiinsulin antibody and receptor binding with liver membrane preparations than intact insulin. Further incubation of A14-125I-insulin with the cytosolar enzyme(s) resulted in reduction of these peaks as well as insulin and formation of 125Iodotyrosine peak. We conclude that human fibroblast is capable of metabolizing cell-associated A14-125I-insulin in a time- and temperature-dependent manner. This process is inhibited by various inhibitors of insulin processing. The bulk of IDA consists of soluble neutral protease(s) with properties similar to other more purified neutral insulin protease preparations. This fraction, similar to the intact fibroblast degrades insulin to two intermediates with similar molecular weight to that of intact insulin but with more hydrophilicity and less binding affinity to antiinsulin antibody and liver membrane than intact insulin.
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PMID:Characterization of insulin-degrading activity of intact and subcellular components of human fibroblasts. 388 99

Human erythrocytes possess a proteolytic activity degrading glucagon (and insulin) even at very low concentrations with a high degree of efficiency. The enzyme which likely belongs to the class of insulin-glucagon-proteinases, can be inhibited by chelating agents, such as ethylenediamine tetraacetic acid and o-phenanthroline, thiol blocking reagents, such as p-chloromercuribenzoate and N-ethylmaleimide as well as by proteinase inhibitors directed against serine proteinases, such as Contrykal and Trasylol. No inhibition could be shown by leupeptin. Insulin in an equimolar range is capable of inhibiting glucagon degradation competitively. Dithioerythritol stimulates the degrading activity. Co++, Zn++, Mn++ and Ca++ prevent the o-phenanthroline mediated inhibition of glucagon degrading activity, whereas Mg++, Cu++, Cd++ and Fe+++ have an inhibitory effect. The glucagon degradation exhibits a pH optimum at 7,1 with an apparent Km of 4.4 X 10(-6) mol/l. The insulin-glucagon-proteinase in human erythrocytes is supposed to have a regulatory influence within the carbohydrate pathway.
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PMID:[Proteolytic degradation of glucagon by human erythrocytes]. 391 53

Oral administration to mice with soybean trypsin inhibitor (SBTI) (27-30 mg/mouse/day) or aprotinin (5500-6000 KIU/mouse/day) for six weeks increased the total pancreatic insulin (IRI). The pancreatic IRI was also increased after sc injections of synthetic caerulein (0.05 microgram/mouse/day divided into 3 daily doses), being 82% above the control levels when expressed per g pancreas. Aprotinin (6000 KIU/mouse/day divided into 3 daily doses) injected sc had no effect on the insulin content. The total glucagon did not change significantly in any of the groups, but the molar ratio of insulin to glucagon was increased in the caerulein- and SBTI-treated mice. Caerulein-treatment led to an increased disappearance rate of glucose with k-values being 7.1 +/- 0.3 compared to 6.0 +/- 0.1 (mean +/- SEM) in the controls (P less than 0.02). In islets isolated by collagenase-digestion of the pancreas and subjected to an overnight incubation, the content of insulin and glucagon was increased in islets from caerulein-treated animals. This corresponded to the results observed in the whole pancreas. The present study suggests that oral administration of proteolytic enzyme inhibitors or treatment with caerulein has a trophic effect on the endocrine pancreas. A difference in specificity seems to exist as SBTI affected both the pancreatic weight and IRI, and aprotinin orally did not influence the pancreatic weight, but increased the total content of IRI. Caerulein led to an increase in IRI, but did not affect the weight of pancreas.
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PMID:Effects of caerulein and trypsin inhibitors on the endocrine mouse pancreas. 616 52


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