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)

Surgical fragments of healthy and tumor-bearing pancreas from a patient with pancreatic tumor were studied by electron or light microscopy, histochemistry, and immunocytochemistry (human insulin, glucagon, somatostatin, gastrin, and bovine pancreatic polypeptide). Histological results were compared to those obtained by radioimmunoassay, both in tumor and serum. The tumor was identified as a glucagonoma because reactions for Grimelius' silver impregnation and immunoreaction with an antiserum against glucagon were positive and because a very high level of glucagon in the tumor was observed. Insulin, somatostatin, and gastrin levels remained normal, both in tumor and serum, but the glucagon level was normal in serum. Associated with this silent glucagonoma, an uncommon nesidioblastosis was also diagnosed with many A cells irregularly mixed with acinar cells, isolated or clustered in small groups. Acinar "intermediate" cells of "A" type were also observed. Such associative histopathological processes evoked possible development of an endocrine tumor from nesidioblastic-like tissue. Its embryogenic origin remained uncertain.
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PMID:Silent human pancreatic glucagonoma and "A" nesidioblastosis. 285 84

Acute effects of somatostatin analog (SMS 201-995) on pancreatic hormones were studied in two patients with malignant islet-cell carcinoma. Before and after subcutaneous injection of somatostatin with a doses of 50 micrograms, blood glucose (BG), serum growth hormone (hGH), C-peptide immunoreactivity (CPR), plasma immunoreactive glucagon (IRG) and gastrin were assayed, and changes in elution patterns of IRG and gastrin were also analyzed on Bio-Gel P-30 column chromatography. In Patient 1 with glucagonoma syndrome and hypergastrinemia, a prompt and remarkable decrease in plasma IRG and gastrin was observed after the injection of SMS 201-995 in association with a decrease in blood glucose, and then IRG and gastrin increased gradually. The suppressive effect continued for at least 6 hours. On gel filtration of the plasma obtained before the injection of the analog, three major peaks, greater than 20000, 9000 and 3500 molecular-weight (mol wt) fractions, were seen in IRG fraction. The decrease in plasma IRG observed at 1 hour after the injection was mainly due to a marked decrease in the 3500 molecular weight fraction. In addition, a slight decrease in the 9000 mol wt fraction was seen. At 4 hours after the injection, the 3500 mol wt peak returned to the previous level, while the 9000 mol wt peak decreased further. On the other hand, the gastrin elution pattern of plasma obtained before the injection revealed three major gastrin peaks, greater than 20000, 7000 and 5000 mol wt fraction. The changes in the gastrin elution pattern after the injection were similar to those of the IRG elution pattern. In Patient 2 with Zollinger-Ellison's syndrome, the plasma gastrin level decreased gradually for 5 hours after the injection. On gel filtration of the plasma obtained before the injection, two major gastrin peaks, 7000 and 5000 mol wt fraction, of which the large-molecular fraction was more prominent than the small-molecular fraction, were observed. After the injection, a marked decrease in the small-molecular fraction and a gradual decrease in the large-molecular fraction were observed for 4 hours, accompanied by a decrease in plasma gastrin. At 7 hours after the injection, the smaller fraction was augmented again. The serum CPR and hGH was slightly suppressed after the injection in both patients. The adverse effects of slight nausea and vomiting were noticed only in Patient 1.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Inhibitory effects of somatostatin analog (SMS 201-995) on pancreatic hormones in patients with malignant islet-cell carcinoma]. 285 26

A patient presenting clinically with the glucagonoma syndrome had high plasma glucagon levels (1920 ng/l) and at laparotomy, a pancreatic islet cell tumour was removed. The tumour was dispersed and placed in culture where it remained viable for 63 days. The tumour cells secreted immunoreactive (IR) glucagon at levels up to 2400 ng/l as detected by a C-terminal glucagon specific antibody and 85 400 ngequiv./l as measured by an N-terminal glucagon specific antibody. The difference between these two levels was attributed to the presence of different molecular forms of glucagon measured with the N-terminal specific antibody. IR insulin (up to 302 mU/l) and IR somatostatin (up to 2500 ng/l) were also detected. There was no direct or inverse correlation between different hormone levels. Small but significant levels of N-terminal and C-terminal vasoactive intestinal peptide (VIP) were detected in some cultures but there was no evidence of gastrin or ACTH. Glucagon and somatostatin secretion persisted for the duration of the culture (63 days) but insulin concentrations declined. Incubation of cultures with somatostatin (1 ng/ml) caused a 75% decrease in glucagon levels, while insulin (1000 mU/l) produced a 70% inhibition of somatostatin.
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PMID:Multiple hormone secretion by a human pancreatic glucagonoma in culture. 286 20

A 63-year-old woman with necrolytic migratory erythema associated with a glucagonoma in the pancreas is described. The diagnosis was suggested on the basis of a characteristic lesion in skin biopsy. Infusion of somatostatin (25 micrograms/h) for 48 hours was followed by a rapid and almost complete healing of the skin eruptions. Serum glucagon was depressed during infusion. No significant changes in plasma glucose were detected. As the patient experienced a cramp-like sensation after cessation of somatostatin infusion, a tail-off period in the infusion program is advocated. The pathogenesis of necrolytic erythema in glucagonoma is discussed.
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PMID:Effect of somatostatin in necrolytic migratory erythema of glucagonoma. 286 72

A 46-year-old man had a 7-year history of severe rash, which was then diagnosed as necrolytic migratory erythema. He had a weight loss of 6 kg, abnormal glucose tolerance test findings, anemia, glossitis, hair loss, and hypoproteinemia. Plasma amino acids levels were significantly decreased, and the fasting plasma glucagon (IRG) level was high at 5000 to 8000 pg/ml. Circulating IRG significantly increased after oral glucose loading, meal ingestion, and arginine infusion, and decreased with somatostatin infusion and insulin-induced hypoglycemia. No other gut or pancreatic hormone levels in plasma were elevated. Plasma IRG was eluted by gel-filtration, mainly in the position of true glucagon (MW 3500) by antiserum 30K. The rash was markedly improved after infusion of amino acids. Computerized tomography (CT) scan and celiac angiography revealed a large pancreatic tumor with multiple liver and lymph node metastases. The pancreatic tumor was totally resected, and was identified as glucagonoma by immunohistochemical technique. Since the plasma IRG levels remained high after surgery, the patient received dimethyltriazenoimidazole carboxamide therapy. After several courses of this treatment, plasma IRG levels decreased to 1000 to 2000 pg/ml, and the hepatic metastases were remarkably diminished in size.
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PMID:A functional study of a case of glucagonoma exhibiting typical glucagonoma syndrome. 286 23

A long-acting somatostatin analog, SMS 201-995, is now available to treat the hormonal manifestations of islet cell tumors. We report its use in a patient with a metastatic glucagonoma refractory to conventional therapy. This patient, who was severely disabled by the rash of necrolytic migratory erythema and brittle diabetes mellitus, allowed us to evaluate the therapeutic efficacy of SMS 201-995 and to gain insight into the origin of the rash. SMS 201-995 was administered subcutaneously (.05 mg twice a day). The rash improved markedly within 48 hours and was completely resolved within 1 week of treatment. Insulin requirements decreased from 90 U/day to zero during the first week of treatment. Corresponding to improvement in clinical symptoms circulating glucagon levels showed a marked decrease. There was no substantial change in plasma or urinary levels of zinc or in plasma amino acid levels. When SMS 201-995 was stopped, the rash recurred within 36 hours and it improved within 48 hours of readministration. The rash and diabetes have remained well controlled during 8 months of therapy but no change in tumor size has been seen on CT scan. The rapid changes in the rash related to the administration of SMS 201-995 indicate that the pathogenesis of necrolytic migratory erythema is probably due to circulating hyperglucagonemia or some other hormonal substance produced by the tumor.
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PMID:Use of a somatostatin analog (SMS 201-995) in the glucagonoma syndrome. 287

A 41-year-old woman with metastatic glucagonoma and the characteristic disabling rash, necrolytic migratory erythema, was treated with a synthetic somatostatin analog while waiting to undergo curative surgical resection. Plasma glucagon concentration (1,500-3,300 pg/ml, normal less than 200) remained elevated during analog therapy as the rash cleared. Only with surgical resection (partial pancreatectomy and partial hepatectomy) did glucagon levels return to normal. The therapeutic benefit caused by the analog in this syndrome differs from that in other endocrine tumor syndromes such as pancreatic cholera, carcinoid, or gastrinoma where circulating levels of tumor-produced agents are suppressed in conjunction with control of symptoms.
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PMID:Somatostatin analog-induced remission of necrolytic migratory erythema without changes in plasma glucagon concentration. 288 3

The glucagonoma syndrome is characterized by a necrolytic migratory erythematous rash, angular stomatitis, painful glossitis, a normochromic normocytic anemia, mild diabetes mellitus, weight loss, a tendency to thrombosis, and neuropsychiatric disturbances. The diagnosis is made by finding a high plasma glucagon concentration in the absence of any other cause, such as renal failure or severe stress. A pancreatic alpha-cell tumor can be identified and stained by immunocytochemistry with glucagon antibodies. Optimal treatment is surgical removal, but approximately 50 percent of the tumors have metastasized by the time of diagnosis. Since the tumor is slow-growing, remission can be obtained by hepatic artery embolization to shrink hepatic secondaries or by shrinkage, in about 10 percent of patients, with the combination chemotherapeutic regimen of 5-fluorouracil and streptozotocin. The rash frequently responds to administration of zinc, a high-protein diet, and control of the diabetes with insulin. Alongside the alpha cell in the islets of Langerhans is the D-cell, which produces somatostatin and may well act physiologically as a paracrine inhibitor of glucagon release. A newly developed, long-acting somatostatin analogue, SMS 201-995, which the patient can self-administer as a subcutaneous injection, has proven effective in suppressing glucagon secretion from glucagonomas and, in some cases, causing remission of clinical symptoms.
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PMID:Glucagonoma syndrome. 288 77

The embryogenesis of the pancreas suggests the existence of a common stem cell progenitor of the four islet cell types (insulin, glucagon, somatostatin, and pancreatic polypeptide). We investigated whether neoplastic islet tumors express multiple hormone-specific cellular phenotypes of the islets. By analyses of RNA transcripts and immunoreactive peptides in four human insulinomas and one glucagonoma, we found that the insulin, somatostatin, and glucagon genes were coexpressed in all tumors. The expression of the three hormone genes in a lymph node metastasis of a glucagonoma reduced the possibility that contamination of tumor tissue by normal islets occurred. These observations lend further support to the hypothesis of the multipotentiality of neoplastic islet cells for the expression of genes encoding several different islet hormones.
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PMID:Expression of peptide hormone genes in human islet cell tumors. 290 36

Alpha cell tumours of the pancreatic islets of Langerhans are rare. The glucagonoma syndrome is caused by excess glucagon secretion from such a tumour. Physiologically, glucagon is important in the control of the homeostatis of glucose and certain amino acids. Pharmacologically, it has been used to treat heart failure. Problems with both glucose homeostasis and myocardial function could, therefore, theoretically be anticipated following resection of a glucagonoma. This paper describes the peri-operative management of such a case, where, despite measured changes in glucagon, no problems of this nature were encountered.
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PMID:Anaesthetic management of glucagonoma. 298 82


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