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)

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

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

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

Immunohistochemical characteristics of a mucinous islet-cell carcinoma of the pancreas are described. The tumour presented with jaundice in a 59-year-old male. It consisted of polygonal atypical cells forming a reticular pattern, and invaded the common bile duct. In DNA flow cytometry, the tumour cells showed a clear-cut aneuploid peak. Intercellular mucin was abundant. A panel of antisera and monoclonal markers was applied in the immunohistochemical analysis. In addition to general epithelial and endocrine markers, the tumour cells showed a focal positive immunoreaction with anti-glucagon, anti-insulin, anti-vasoactive intestinal polypeptide, anti-pancreatic secretory trypsin inhibitor and anti-phospholipase A2 antigen. At the ultrastructural level, mucous and neuroendocrine granules were demonstrated in the same tumour cells.
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PMID:Immunohistochemical characterization of an amphicrine mucinous islet-cell carcinoma of the pancreas. Case report. 131 30

Twenty-three patients with obstructive jaundice were given a 50-g oral glucose tolerance test (G.T.T.) and an insulin stimulation test with oral glucose and intravenous tolbutamide and glucagon. An abnormal glucose response was as common in patients with carcinoma of the pancreas (seven out of 12) as in patients with "other" causes of obstructive jaundice (six out of 11). Though both groups had a low and delayed insulin response the insulin levels were significantly lower in patients with carcinoma of the pancreas. After the insulin stimulation test patients with obstructive jaundice who did not have carcinoma of the pancreas had a greater and significantly different insulin response from patients with pancreatic cancer. There was, however, considerable overlapping between the results of individual patients in the two groups.
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PMID:Carbohydrate tolerance and insulin responses in obstructive jaundice. 442 18

A patient with glucagonoma syndrome and hypoglycemic attack is presented. Total pancreatectomy was performed with splenectomy and excision of the metastatic nodule in the liver. Diagnosis of glucagon-secreting A cell carcinoma of the pancreas was confirmed by hormone assays and morphological studies with light and electron microscopy. Glucagon, insulin, and somatostatin were demonstrated immunohistochemically in the tumor tissue. Multihormonal features of the endocrine pancreatic tumors are discussed.
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PMID:Glucagon-secreting pancreatic islet cell carcinoma, containing insulin and somatostatin, with hypoglycemic attack. 612 21

A case of pancreatic carcinoma with both acinar and endocrine features is presented. The patient was a 52-year-old female presenting with jaundice of 3 weeks' duration. The tumor was a 6 x 6 cm-sized round solid mass in the head of pancreas, invading the superior mesenteric vein. Histologically, it was composed of monotonous ovoid cells with eosinophilic granular cytoplasm in solid nests and sheets with occasional acinar and glandular differentiation. Immunohistochemical study revealed coexpression of acinar and endocrine markers; amylase, chromogranin, neuron-specific enolase, glucagon, somatostatin, and gastrin in tumor cells. This is the first documented case of mixed acinar-endocrine carcinoma of the pancreas in Korea, and its amphicrine nature reflects a close histogenetic relationship between pancreatic exocrine and endocrine cells.
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PMID:Mixed acinar-endocrine carcinoma of the pancreas--a case report. 883 69

A pancreatic carcinoma, associated with elevated serum alpha-fetoprotein level, was resected from a 67-year-old man. The tumor was strongly suggested to be an acinar cell carcinoma of the pancreas, based on the histological findings of the resected specimen. The tumor measured 12 x 10 x 9 cm, and the cut surface was soft, whitish-yellow, focally necrotic, and hemorrhagic. Under a light microscope, the tumor cells were not arranged in a tubular and trabecular pattern, but rather, showed a tendency toward an acinar structure. Immunohistochemically, alpha 1-antitrypsin- and alpha 1-antichymotrypsin-positive reactions were diffusely positive in most of the tumor cells, while staining for chromogranin, neuron-specific enolase, Grimelius, glucagon, insulin, and alpha-fetoprotein was negative in the tumor cells. We report a large acinar cell carcinoma (associated with elevated serum alpha-fetoprotein level), which had been misdiagnosed as hepatocellular carcinoma preoperatively.
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PMID:Large acinar cell carcinoma of the pancreas in a patient with elevated serum AFP level. 1098 18

Pancreatic carcinoma is characterized by poor prognosis and lack of response to conventional therapy for reasons that are not clear. Because of the structural relationship between the exocrine and endocrine pancreas and high concentrations of islet hormones bathing pancreatic tissue, we hypothesized that pancreatic cancer cell proliferation and glucose utilization are regulated by pancreatic islet hormones, particularly insulin. Based on this, the effect of islet hormones on pancreatic cancer cells in vitro was investigated. Five pancreatic cancer cell lines, CD11, CD18, HPAF, PANC-1, and MiaPaCa2 were used to investigate the effect of islet hormones on cell proliferation, glucose utilization, and GLUT-1 expression. Insulin, but not somatostatin and glucagon, induced pancreatic cancer cell growth in a concentration- and time-dependent manner. At concentrations within the range of those in the intrapancreatic vasculature, insulin (10(-10)-10(-8) mol/L) markedly increased [3H]-thymidine incorporation. Insulin significantly enhanced glucose utilization of pancreatic cancer cells before it enhanced cell proliferation. The MAPK kinase inhibitor PD 098059 abolished insulin-stimulated DNA synthesis and partially reduced insulin-stimulated glucose uptake. In contrast, the PI3 kinase inhibitor wortmannin substantially inhibited insulin-induced glucose uptake and partially blocked thymidine incorporation. Furthermore, after 24-hour treatment with insulin, GLUT-I expression in pancreatic cancer cells was markedly increased, indicating that insulin enhances glucose utilization partly through increasing glucose transport. These findings suggest that insulin stimulates proliferation and glucose utilization in pancreatic cancer cells by two distinct pathways. Insulin augments DNA synthesis mainly by MAP kinase activation and glucose uptake mainly by PI3 kinase activation and enhancement of GLUT-I expression. High intrapancreatic concentrations of insulin are likely to play an important role in stimulating pancreatic cancer growth indirectly by increasing substrate availability as well as by direct action as a trophic factor.
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PMID:Physiological concentrations of insulin augment pancreatic cancer cell proliferation and glucose utilization by activating MAP kinase, PI3 kinase and enhancing GLUT-1 expression. 1103 77

We report a patient with insulinoma associated with Zollinger-Ellison syndrome. A 67-year-old woman was first admitted to our hospital for an abdominal mass. Abdominal computed tomography (CT) revealed a large pancreatic tumor, which was then diagnosed as an unresectable pancreatic adenocarcinoma. At the age of 71, she presented symptoms of hypoglycemia. Fasting blood glucose was 21 mg/dl and plasma immunoreactive insulin level was 846 microU/ ml. Plasma gastrin, glucagon, vasoactive intestinal polypeptide and somatostatin levels were all normal. At the age of 73, hypoglycemic attacks occurred more frequently and she was admitted to our hospital. Abdominal CT scan showed multiple liver metastases. Chemotherapy with 5-fluorouracil and doxorubicin was performed. Three months later, she had an emergency laparotomy because of a perforated duodenal ulcer. Plasma gastrin level was 1,960 pg/ml at that time. Gastric hypersecretion was well controlled with a proton pump inhibitor (lansoprazole) but she died of widespread cancer dissemination 8 years after her first admission. On autopsy, histologic examination revealed a mixed acinar-endocrine carcinoma of the pancreas. Immunohistochemical stains were positive for insulin, gastrin, and alpha1-antitrypsin.
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PMID:Insulinoma with subsequent association of Zollinger-Ellison syndrome. 1139 7


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