Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of diabetes due to chronic pancreatitis would appear to be increasing. In western countries this is associated with the known increase in alcohol consumption and AIP. Malnutrition may be etiologic in tropical areas. The incidence of diabetes in chronic pancreatitis is dependent on a number of factors. It is more common in alcohol-induced pancreatitis, rarely occurs after the first attack but tends to increase with time and rises markedly in calcific pancreatitis. Abnormal glucose tolerance occurred in 91% of patients with calcific pancreatitis and 70% of patients with noncalific AIP in our follow up of five to 12 years. This stresses the importance of serial regular glucose tolerance tests in these patients (Table I). The insulin-reserve is severely depleted in most patients who do not yet demonstrate abnormal glucose tolerance, indicating that pancreatitis regularly affects the islets and that nearly all patients are potential diabetics. The beta cells appear to respond better to oral glucose, glucagon or secretin than to i.v. glucose suggesting a selective glucose receptor loss or block to hyperglycemia in chronic pancreatitis. The alpha cells seem to be more resistant to the effects of chronic pancreatitis but true hypoglucagonemia was found in 16% of patients. In addition, stimulated growth hormone secretion may be deficient in pancreatic diabetes. These last two factors, among others, may be responsible for the protracted and even fatal hypoglycemia to which some patients with AIP on insulin therapy are liable. The danger of drug-induced hypoglycemia, coupled with the infrequency of vasculopathy, retinopathy and nephropathy in pancreatic diabetes has induced us to keep these patients hyperglycemic and glycosuric rather than in a sugar-free state, as long as symptoms are contained. Recurrent abdominal pain, marked weight loss and associated steatorrhea often raise special problems in the management of the pancreatic diabetic.
 ...
PMID:Clinical and hormonal aspects of pancreatic diabetes. 80 21

In dogs with acute experimental pancreatitis (AEP) induced according to Elliotts method the total, free and latent activity of lysosomal hydrolases (acid phosphatase, beta-glucuronidase and cathepsins) in whole homogenates and some subfractions of pancreas were studied. The animals were divided into three groups of 6 dogs each: I. control healthy dogs. II. AEP-treated with glucagon (0.33 mg of glucagon in drop infusion 3 times every six hours). III. AEP without any drug treatment. In dogs treated with glucagon the significant decrease of relative free activity of all tested hydrolases (66-80%) in comparison with the group without any treatment (III/80-90%) was found. Moreover significant decrease of total catheptic activity (about 1/3) in the former group was demonstrated. Incubation of lysosomal enriched fraction taken from group II/in medium buffered to pH 5.0 caused decreasing release of catheptic activity (60% of total) in comparison with the group III (75%). The histochemical reaction for acid phosphatase according to Gomoris method in pancreatic acinar cells of dogs treated with glucagon was less intensive than reaction in untreated animals. These results indicate on the less impairment of pancreatic lysosomes in AEP treated with glucagon in comparison with that in untreated animals.
 ...
PMID:The lysosomal hydrolases in acute experimental pancreatitis in dogs treated with glucagon. 84 47

Unmodified synthetic somatostatin, given as a 200-microgram intravenous bolus, plus 200 microgram infused over 3 hours, had no effect on basal plasma insulin and pancreatic glucagon-like immunoreactivity (GLI) levels, both in controls and in patients with chronic pancreatitis. Somatostatin inhibited insulin-hypoglycaemia-induced pancreatic GLI release in controls and in patients with pancreatitis, and prolonged the insulin-induced fall in blood glucose in the patients. Arginine, presumably via insulin release, caused a fall in free fatty acids (FFA) in controls, which was inhibited by somatostatin. Somatostatin abolished the rebound rise in plasma FFA in patients with pancreatitis after insulin-hypoglycaemia. This effect may be related to inhibition of pancreatic GLI release or may be a direct action of somatostatin on lipolysis.
 ...
PMID:The effects of somatostatin on hormonal and metabolic responses in chronic pancreatitis. 89 37

This study was designed to assess the value of glucagon infusion in pigs with experimental pancreatitis. The condition was induced by injection of bile into the pancreatic duct directly after intravenous injection of secretion. Macroscopic haemorrpagic pancreatitis ensued immediately, and was accompanied by a rise in the serum amylase of five to ten times. An experimental group of 15 pigs was given glucagon by continous infusion for 18 hours beginning 18 hours after induction of pancreatitis. A control group was given intravenous saline. Fourteen of the 15 treated animals survived for 1 week and 3 died within 2 weeks, after which the remaining animals were sacrificed. Ten of the 15 controls died within the first week. Serum amylase levels in both groups began to decline when infusion was commenced, but levels in the treated group were significantly lower than in the controls. Autopsy showed prominent peripancreatic granulation tissue in the treated animals, a significant incidence of pericarditis in both groups and pancreatic pseudocysts in 3 controls and 1 treated animal. These results suggest that glucagon effectively reduced the mortality in pigs with experimental pancreatitis and that a controlled clinical trial of treatment is justified.
 ...
PMID:A conrolled trial of glucagon in experimental pancreatitis. 95 66

Serial measurements of plasma "true glucagon" (PG) and of glucagon-like immunoreactive materials (GLI) were carried out during and after total resection of the pancreas in a 62-year-old man with calcified pancreatitis. The postoperative course of this patient was uneventful and diabetes was well controlled. PG disappeared from the blood within 30 min after resection of the pancreas. In spite of the evidence that no pancreatic tissue was present in the abdomen, PG was detected again in the blood from 18 hr after total pancreatectomy until the ninth postoperative day. However, plasma PG did not rise following infusion of arginine during the fourteenth postoperative week. After an initial decrease, plasma GLI rose abruptly on the second postoperative day and remained elevated thereafter. The fluctuations of plasma PG and GLI were not parallel.
 ...
PMID:Plasma glucagon after total resection of the pancreas in man. 96 83

The effects of tolbutamide infusion (1 gm. over forty minutes) on plasma pancreatic glucagon-like immunoreactivity (PGLI), serum insulin, and blood glucose were studied in six patients with chronic pancreatitis and six matched controls.asal PGLI levels were significantly higher in the patients, despite higher fasting glucose concentrations. Tolbutamide infusion had no significant effect on mean PGLI levels in controls but was associated with significant elevation in pancreatitis patients, despite higher circulating glucose levels in the latter. The data suggest that chronic calcific pancreatitis patients hypersecrete immunoreactive glucagon, possibly from a nonpancreatic source and that this immunocreactive material may be stimulated by sulfonylureas.
 ...
PMID:Immunoreactive glucagon responses to intravenous tolbutamide in chronic pancreatitis. 115 44

Thyrocalcitonin release mediated by glucagon secreted from the acutely inflamed pancreas has been postulated as a possible mechanism for hypocalcemia in acute pancreatitis. To test this hypothesis, hemorrhagic pancreatitis was induced in a group of thyroidectomized pigs. No source of thyrocalcitonin other than the thyroid has been described in the pig. Their subsequent serum calcium concentrations were compared with those in a group of thyroid intact pigs also given hemorrhagic pancreatitis. The results indicate that the hypocalcemia observed during the first 24 hours following induction of pancreatitis is not related to the presence of an intact thyroid. Differences observed in the degree of hypocalcemia between the two groups 30 to 48 hours after pancreatitis developed may be of significance but could be explained by dilutional differences alone. Thyrocalcitonin apparently has little if any role in the hypocalcemia observed during the course of acute pancreatitis.
 ...
PMID:Mechanisms of hypocalcemia in acute hemorrhagic pancreatitis. 119 6

Plasma pancreatic glucagon concentrations were determined in the basal state and after the infusion of alanine in 10 patients with acute pancreatitis (5 in an initial episode of pancreatitis), in 10 patients with chronic pancreatic insufficiency, and in 21 healthy controls. In acute pancreatitis, basal glucagon levels were nine times normal but were higher during the initial attack than with a history of previous attacks. The glucagon response to alanine was also increased threefold to fourfold in initial attacks. In contrast, after recovery from the initial attack of acute pancreatitis, during acute episodes of pancreatitis in patients with a history of previous attacks, and in patients with pancreatic insufficiency, alanine failed to elicit a consistent rise in plasma glucagon. The data suggest that hyperglucagonemia may contribute to the hyperglycemia of acute pancreatitis, particularly during the initial episode. Loss of alpha cell responsiveness to alanine provides a sensitive index of previous pancreatitis.
 ...
PMID:Glucagon secretion in acute and chronic pancreatitis. 120 May 23

CFY male rats anaesthetized with pentobarbital were used in different groups for inducing acute pancreatitis by the retrograde injection either of 1 mg elastase, 5 mg trypsin, 4 mg lysolecithin, 10 mg Na-taurocholate in 0.2 ml volume or of 0.3 m. sunflower oil. In each group laparatomized animals served for control. The animals with pancreatitis were treated either with 15 mug/b.w.kg/hour glucagon or with physiological saline for 72 hours. Twenty-four and 72 hours after inducing pancreatitis glucagon did not influence the significant fall in blood pressure elicited by the intraductal injection of trypsin or elastase or in the plasma calcium level in pancreatitis induced by trypsin or sunflower oil. Neither did glucagon affect the significant increase of plasma lipase activity in pancreatitis induced by trypsin or taurocholate. It also failed to reduce the 24-hour mortality rate and the extension of fat tissue necrosis in the abdominal cavity of pancreatitic animals. In contrast, glucagon treatment significantly reduced the amount of abdominal exudate associated with bile salt induced pancreatitis and, probably due to its pancreatic blood flow increasing effect, seemed to moderate the degree of tissue damage elicited in the pancreas by detergents such as taurocholate or lysolecithin.
 ...
PMID:Glucagon treatment of experimental acute pancreatitis. 123 17

The plasma gastric inhibitory polypeptide (GIP), pancreatic glucagon-like immunoreactivity (PGLI), and gut glucagon-like immunoreactivity (GGLI) responses to oral glucose have been measured in five patients with chronic pancreatitis (with diabetic glucose tolerance tests) and in matched nondiabetic controls. Plasma GIP levels rise rapidly after glucose ingestion before changes in circulating glucose and insulin concentration. Patients with pancreatitis have a greater than normal GIP response to oral glucose, which may account for the relatively unimparied insulin response to oral glucose in these patients compared with that to iv glucose, as has been previously found. Patients with pancreatitis also have a paradoxical rise in PGLI and an exaggerated rise in GGLI concentration following oral glucose.
 ...
PMID:Gastric inhibitory polypeptide (GIP) in chronic pancreatitis. 127 May 74


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>