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)

In the plasma of healthy subjects, 4 fractions of immunoreactive glucagon are found. The first has a molecular weight of about 160000, the second of 9000, the third 3500 and the fourth about 2000. The third probably corresponds to the intact hormone glucagon. In cirrhosis of the liver and diabetes mellitus, a statistically significant rise in the third fraction has been found. In patients with tumors of the pancreatic A-cells, in addition to the third fraction the second in particular was also increased: it may be a precursor of the glucagon molecule. In chronic renal insufficiency, fractions 2 and 3 were as markedly increased as in glucagonoma, which suggests a role for the kidney in the decomposition of glucagon. The pathophysiologic significance of the four immunoreactive fractions of glucagon cannot yet be assessed with certainty.
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PMID:[Circulating types of human glucagon (author's transl)]. 30 29

Five tumors associated with the complete glucagonoma syndrome, as well as a series of glucagon-cell adenomas from three patients without this syndrome, were investigated by light and electron microscopy and by immunofluorescence. All tumors associated with the syndrome were large, from 3 to 35 cm along the major axis, and three of them were proved to be malignant. No common histologic arrangement of tumor cells was apparent for the five neoplasms examined. Immunofluorescent staining for glucagon and glicentin was carried out: while most cells were negative, a varying number of scattered cells were positive with both antisera in all tumors except one; three tumors contained more glicentin- than glucagon-immunoreactive cells. Moreover, three tumors were multihormonal, witn cells positive for pancreatic polypeptide and/or insulin. Ultrastructurally, the secretory granules of cells from these tumors were not typical of those found in A-cells from adult human islets. The glucagon-cell tumors from patients without the syndrome were benign, usually multiple, and were small, with diameters from 0.5 mm to 1 cm. In most cases, the cells from these neoplasms arranged in a characteristic pattern (ribbonlike or "gyriform"). In most tumors, the majority of cells showed both glucagon and glicentin immunofluorescence and the ultrastructural appearance of their secretory granules was similar to that of normal islet A-cells. From the morphologic point of view, therefore, cells from tumors not associated with the glucagonoma syndrome resemble normal glucagon cells more closely than those from tumors associated with the syndrome.
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PMID:A study of glucagonomas by light and electron microscopy and immunofluorescence. 38 56

A 54-year-old male with diabetes, weight loss, glossitis and Candidiasis presented with the typical cutaneous eruption of necrolytic migratory erythema. The suspicion of pancreatic glucagonoma was confirmed by an elevated plasma glucagon level. Surgical removal of the pancreatic alpha cell tumor resulted in a complete disappearance of all symptoms. The importance of the recognition of the skin eruption of necrolytic migratory erythema as a clue to the presence of pancreatic glucagonoma is emphasized.
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PMID:Necrolytic migratory erythema, presenting as candidiasis, due to a pancreatic glucagonoma. 47 69

Necrolytic migratory erythema is the distinctive cutaneous eruption seen with glucagon-producing tumours of the pancreas. Recognition of this eruption is important because it may lead to the early diagnosis of a glucagonoma. Recently, we saw a patient who had necrolytic migratory erythema, hyperglucagonaemia, and cirrhosis of the liver with no evidence of pancreatic tumour while alive or at autopsy. Serum glucagon levels during the period of observation and during an oral glucose tolerance test suggested that the hyperglucagonaemia was not due to an occult glucagon-producing tumour but may have been the result of advanced hepatic cirrhosis.
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PMID:Hyperglucagonaemia and necrolytic migratory erythema in cirrhosis--possible pseudoglucagonoma syndrome. 51 28

A 66-year-old male patient with non-insulin-dependent diabetes of probably 20 years' duration presented with necrolytic migratory erythema, stomatitis, anemia and weight loss. Plasma-glucagon concentration measured with Unger's antibody 30-K was 8500 pg/ml, representing a hundredfold elevation. Two thirds consisted of high molecular glucagon fractions (10 000--40 000 Dalton). This may be an important index for detection of glucagonoma with endocrine activity. After excision of the glucagonoma the clinical syndrome was reversed and the patient recovered completely. Histological and histochemical investigation confirmed that the tumor was a glucagonoma. Despite complete removal of the tumor and a normal plasma glucagon concentration, the diabetes remained unchanged. Excessive hyperglucagonemia does not appear to play a primary role in the pathogenesis of this patient's diabetes.
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PMID:[The course of diabetes and clinical findings in glucagonoma]. 52 94

In this paper two patients with uncommon syndromes, viz. acrodermatitis enteropathica-like eruption due to acute zinc deficiency, when on long-term intravenous hyperalimentation for Crohn's disease, and necrolytic migratory erythema as a consequence of a malignant glucagon secreting alpha-cell tumour of the pancreas (glucagonoma syndrome) are reported. Attention is paid to the many common features of the skin lesions in both syndromes. This is discussed in detail. Both patients passed through a catabolic stage. Laboratory investigations, however, failed to demonstrate a common biochemical mechanism which might be responsible for the skin lesions. Administration of zinc in the first patient and surgical treatment of the second patient results in rapid clearing of the skin lesions and other symptoms.
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PMID:Zinc deficiency syndrome versus glucagonoma syndrome. 53 35

The endocrine function of the pancreas consists of the promotion of storage of nutritive substances after meals through the liberation of insulin and to guarantee the mobilization of this food energy through the secretion of glucagon during fasting. Increased hormone production may result from tumors of the islet cells (insulin: insulinoma; glucagon: glucagonoma; gastrin: Zollinger-Ellison syndrome). An absolute or relative insulin deficiency is a characteristic of diabetes mellitus, in which a relative hyperglucagonemia is also of possible pathophysiological significance. This increased secretion of glucagon can be suppressed by somatostatin. While the clinical application of somatostatin in diabetes mellitus seems problematic at present, the use of a glucose-controlled system of insulin infusion ("artificial pancreas") makes possible a metabolic state approaching the healthy condition.
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PMID:[The endocrine pancreas. From the isolated islet to the "artificial pancreas" (author's transl)]. 81 14

In two patients with the glucagonoma syndrome, percutaneous transhepatic puncture of the portal vein and catheterization of the pancreatic veins were performed simultaneously with catheterization of the inferior vena cava and abdominal aorta. Blood samples obtained from the vena cava, aorta and portal branches were assayed for glucagon. In both patients, clearcut arteriovenous glucagon differences allowed preoperative localization of the tumors. A comparison with other localization techniques, such as scintiscan, ultrasound, arteriography and pancreatic phlebography, showed the present method to be superior. Postoperatively, the same investigations were performed revealing arterial and venous glucagon levels comparable to the levels measured in a reference group of three patients without glucagonomas. The triple catheterization technique is advocated for all patients with clinical and laboratory findings that suggest pancreatic endocrine tumors.
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PMID:Localization of glucagonomas by catheterization of the pancreatic veins and with glucagon assay. 89 72

The endocrine cells of the pancreas develop from the endoderm and yet display several characteristics of a neuronal phenotype. During embryonic life, ductal epithelial cells give rise to first the glugagon-producing cells (alpha-cells) and then cells that express insulin (beta-cells), somatostatin (delta-cells), and pancreatic polypeptide (PP-cells) in a sequential order. The endocrine cells are believed to arise from a stem cell with neuronal traits. The developmental lineage from a common neuron-like progenitor is evidenced by: transient coexpression of more than one cell type-specific hormone in immature cells, expression of neuronal markers during islet cell development, and the pluripotentiality of clones of insulinoma cells to develop into cells expressing other islet cell hormones. The four mature endocrine cell types assume a particular organization within the islets of Langerhans in a process where cell adhesion molecules are involved. In this study we have analyzed the expression of neural cell adhesion molecule (NCAM) and cadherin molecules in neonatal, young, and adult rat islet cells as well as in glucagonomas and insulinomas derived from a pluripotent rat islet cell tumor. Whereas primary islet cells at all ages express unsialylated NCAM and E-cadherin, as do insulinomas, the glucagonomas express the polysialylated NCAM, which is characteristic for developing neurons. The glucagonomas also lose E-cadherin expression and instead express a cadherin which is similar to N-cadherin in brain. Insulinoma cells express E-cadherin but differ from primary islet cells by expressing a second cadherin molecule, which is similar to N-cadherin. The expression of NCAM and cadherin isoforms in the glucagonoma suggest that this transformed alpha-cell type has converted to an immature phenotype with strong neuronal traits, reflecting the early palce of glucagon-producing cells in the islet cell lineage. In contrast, insulinoma cells are more islet-like in their phenotype and show less neuronal traits.
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PMID:Differential expression of neural cell adhesion molecule and cadherins in pancreatic islets, glucagonomas, and insulinomas. 140 10

Stable-isotope methodology and indirect calorimetry were used to evaluate metabolic abnormalities in a patient with glucagonoma syndrome manifested by 17% body weight loss, hypoaminoacidemia, and hyperglycemia. Energy expenditure (26 kcal/kg) was the same as that predicted by the Harris-Benedict equation. The rate of appearance (Ra) of intracellular leucine (2.70 mumol/kg/min), an index of protein breakdown, was normal, although the percentage of leucine flux oxidized (31%), an index of amino acid catabolism, was 50% greater than the normal mean value. Glucose Ra in plasma (12.9 mumol/kg/min), representing hepatic glucose production, and glycerol Ra in plasma (3.04 mumol/kg/min), a measurement of whole-body lipolysis, were 15% and 25% greater, respectively, than mean values found in normal volunteers. These results suggest that long-term alterations in energy, leucine, glucose, and lipid metabolism in patients with glucagonoma are minimal. However, small long-term metabolic alterations caused by glucagon excess, in conjunction with chronic negative energy balance, could be responsible for the weight loss, hypoaminoacidemia, and hyperglycemia observed in this patient population.
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PMID:In vivo assessment of the metabolic alterations in glucagonoma syndrome. 143 87


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