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)

A 36-year-old man suffering from chronic pancreatitis involving the whole organ had total duodenopancreatectomy. The Langerhans' islets were isolated from the extirpated organ and transplanted into the liver via portal artery. Insulin substitution could be lowered from 50 I.U. to 12 I.U. by the 5th post operative day. Repeatedly, raised insulin levels could be verified in response to high blood sugar loads. C-peptide and glucagon were also found. 7 months after transplantation the islets still seem to be functioning.
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PMID:[Autotransplantation of Langerhans' islets in a case of total duodenopancreatectomy (author's transl)]. 12 Apr 74

Angiography before and after the administration of Glucagon was performed in 33 adult patients with symptoms suggesting a pancreatic lesion. Preferently the pancreatographic effect was evaluated. The results were compared with those of the angiography following the administration of Secretin and Tolazoline. The pancreatographic effect was visualized in 70% of the patients examined with Glucagon and the rate of visualization of the effect with Secretin and Tolazoline was 60% and 74.5% respectively. The representation of the small vessels could be enhanced with Glugacon only in 15% for the arteries and in 12.5% for the veins, whereas using Secretin and Tolazoline the improvement raised up to 78% of the cases. -- The pancreatographic effect as an additional sign is useful in the differential diagnosis of the chronic pancreatitis (mottled) and the carcinoma of the pancreas (defect or absence of the effect).-- The superselective technique is recommendable. Using this method an improvement of the pancreatographic effect can be achieved already. In pharmacoangiography Tolazoline gives better results than Glucagon.
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PMID:[The pancreatographic effect during pharmacoangiography of the pancreas following the administration of glucagon (author's transl)]. 13 54

The endocrine pancreatic tissue from patients with severe primary chronic pancreatitis (n=6). secondary chronic pancreatitis due to duct obstruction by carcinoma (n=6) and non-diabetic, non-pancreatitic controls (n=4) was studied qualitatively and quantitatively using specific immunocytochemistry and electron microscopy. Grouping of variously sized islets in the sclerotic tissue (sclerosis islets), islet neoformation by ductuloinsular proliferation, and intrainsular fibrosis were the main qualitative findings. Immunocytochemical quantitation of the distribution of insulin (B), glucagon (A), somatostatin (D) and pancreatic polypeptide (PP) producing cells revealed a significant relative increase in the number of A cells and a decrease in the number of B cells of the sclerosis islets in primary chronic pancreatitis ((B-44.1+/-9.3%:A-38.3+/-2.4%:D-8.6+/-5.1%:PP-4.6+/-4.1%) as well as in secondary chronic pancreatitis B-38.0+/-14.3%:A-38.4+/-19.0%:D-9.1+/-5.8%:PP-14.5+/-23.4%) compared with controls (B-71.1+/-8.1%:A-24.3+/-5.5%:D-8.0+/-2.8%:PP-0.5+/-0.4%). The number of PP cells was significantly increased in primary chronic pancreatitis only. It is suggested that scarring of the exocrine pancreas affects islet composition, probably by impairment of the local circulation and of glucose diffusion, thus leading to reduction of the number and glucose sensitivity of B cells. The hyperplasia of A and PP cells appears to be a secondary phenomenon due to the loss of B cells.
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PMID:The endocrine pancreas in chronic pancreatitis. Immunocytochemical and ultrastructural studies. 14 59

17 oral glucose tolerance tests with simultaneous estimation of plasma insulin, were carried out in 15 patients with chronic pancreatitis of which 7 were of calcific type. Among these patients, 10 had obvious diabetes and 3 chemical diabetes. The disorders of glucose regulation were more common in the calcific form of the disease. Serum insulin was then lower and not stimulant. The curves of plasma insulin obtained in non-calcific pancreatitis were variable. In hyperinsulinism, the oral glucose tolerance test showed flat or normal curves. In hypoinsulinism, the glucose tolerance tests were either normal or strongly pathological. This insulinism, as shown by this study of chronic pancreatitis, seems to be linked to an imbalance in the cell distribution of the islets of Langerhans. The role of glucagon appears preponderant.
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PMID:[Study of insulin secretion in chronic pancreatitis]. 18 95

Angiographic findings in one giant cell carcinoma, one cystadenocarcinoma, one poorly vascularized mucinous cystadenocarcinoma, as well as in two avascular (gastrin- and glucagon-producing) islet-cell tumors of the pancreas are described. Two hypervascularized islet-cell tumors are presented for comparison and a case of tumorous chronic pancreatitis in a child is reported because ot its rarity. The aggressiveness of the giant cell carcinoma of the pancreas was demonstrated by its expansive growth. In the case of cystadenocarcinoma angiography revealed the tumor with hepatic metastases not diagnosed at explorative laparotomy. The relative hypovascularity in the case of mucinous cystadenocarcinoma was unusual. Both avascular islet-cell tumors simulated a pancreatic pseudocyst and the final diagnosis was made only by immunoassay. Chronic pancreatitis in a child presented with marked hypervascularization.
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PMID:Angiographic findings in some rare pancreatic tumors. 18 40

Plasma cyclic AMP levels were determined during a 40 minute secretin infusion (1 Cl.U kg-1h-1) followed by a 40 minute combined secretin (1 Cl.U kg-1h-1) caerulein (75 ng kg-1h-1) infusion. In nine healthy subjects, both secretin alone and secretin in combination with caerulein did not affect plasma cyclic AMP levels. The same was observed in six patients with chronic pancreatitis. By contrast, in patients suffering from liver disease (nine cases) or extrahepatic cholestasis (six cases), secretin elicited large increases in plasma cyclic AMP concentration; the mean values attained being, respectively, seven and four times higher than before the infusion. On the other hand, increases in plasma cyclic AMP 10 minutes after a bolus injection of glucagon (1 mg) were four times lower in the liver disease group as compared to the controls. The results reported here suggest that the liver plays a major role in the degradation of plasma cyclic AMP produced by target tissues responding to secretin, and in the release of cyclic AMP under glucagon. Liver disease reduce the capacity of the liver to clear cyclic AMP from the blood. The pancreas does not contribute significantly to the cyclic AMP in the blood.
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PMID:Plasma cyclic AMP levels during a secretin-caerulein pancreatic function test in liver and pancreatic disease. 20 44

Plasma insulin, pancreatic glucagon and immunoreactive glucagon-like polypeptide of intestinal origin (enteroglucagon) have been measured in 10 patients with chronic pancreatitis and 5 normal subjects. Basal levels and changes following oral glucose (50 g) and an intravenous infusion of arginine (25 g in 30 min) have been studied. In patients with chronic pancreatitis the plasma insulin response to oral glucose and intravenous arginine was reduced. Basal pancreatic glucagon was increased in the patients and increased further with oral glucose. During an arginine infusion the pancreatic glucagon showed a brisk early increase greater than that seen in the normal subjects. Basal enteroglucagon levels were significantly increased in chronic pancreatitis but response to orla glucose and arginine infusion were little different from those seen in the normal subjects.
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PMID:Glucagon secretion in chronic pancreatitis. 38 67

A reliable, sensitive, reproducible and specific radioimmunoassay for cholecystokinin-pancreozymin (CCK) has been developed, using rabbit antisera to highly purified porcine hormone. The natural occurring variant of CCK (39-CCK), in which the ordinary CCK is lengthened from its N-terminus by a hexapeptide, labelled with 125J, and repurified by column chromatography on Sephadex G-10 and on SP-Sephadex C-25, was used as tracer. Separation from antibody-bound labelled 39-CCK was carried out using a double antibody procedure. Non-specific interference with the assay system was abolished by ethanol extractions. Highly purified porcine CCK was used as standard. No significant crossreaction was found with gastrin, motilin, vasoactive polypeptide (VIP), gastric inhibitory polypeptide (GIP), natural and synthetic secretin, pancreatic glucagon or insulin. The sensitivity of the assay is approximately 40 pg/ml of test solution. The mean immunoreactive CCK concentration in 45 fasting normal subjects was 222 pg/ml increasing after food ingestion to 480 pg/ml. Somatostatin was able to abolish the stimulated CCK release. Elevated CCK concentrations were found in chronic pancreatitis. Immunohistochemical identification of pancreozymin cells was carried out either in surgical samples or in biopsy material. Approximately 1650 CCK cells per cross-section in the duodenum of humans have been found. The CCK cells usually appeared elongated, oval or pyramidal in shape and were observed to reach the lumen with their apical cell pole.
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PMID:Estimation of cholecystokinin-pancreozymin (CCK) in human plasma and tissue by a specific radioimmunoassay and the immunohistochemical identification of pancreozymin-producing cells in the duodenum of humans. 56 41

Oral glucose administration caused an exaggerated release of cross-reacting gastrointestinal glucagon-like immunoreactivity (GLI) and a slight early rise in immunoreactive glucagon (IRG) concentration in patients with chronic pancreatitis, who have impaired insulin release. Intravenous administration of 200 microgram of somatostatin, followed by infusion of 200 microgram over 2 1/2 h, abolished the GLI and insulin responses, but did not change glucose tolerance. This contrasts with the relatively minor effects of somatostatin on GLI responses in control subjects where the clear deterioration in glucose tolerance may relate to inhibition of insulin release.
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PMID:Inhibition of exaggerated gastrointestinal glucagon responses in chronic pancreatitis by somatostatin. 59 21

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


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