Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

A case of a 58-year-old woman with an unusual variant of malignant islet-cell tumor showing oncocytic features is described. Using the light microscopy technique, the tumor appeared comprised of solid nests of uniform cells with abundant, eosinophilic cytoplasm and round nuclei with granular chromatin. Ultrastructurally, the cells contained numerous abnormal mitochondria, dilated rough endoplasmic reticulum, and scattered dense-core neurosecretory granules, often associated with cytoplasmic filaments. Tumor cells were focally immunoreactive for insulin, glucagon, and somatostatin and diffusely immunoreactive for alpha 1-antitrypsin as assayed by the avidin--biotin technique. The tumor was immunonegative for human chorionic gonadotropin, gastrin, adrenocorticotropic hormone, and serotonin. The patient exhibited some of the clinical features associated with glucagonoma syndrome, including diabetes mellitus and chronic diarrhea. The tumor behaved in a malignant fashion, with widespread lymphatic involvement and bony metastases at the time of presentation. This report of an oncocytic islet-cell carcinoma supports the concept of oncocytic differentiation in islet-cell tumors in a fashion analagous to oncocytic carcinoids.
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PMID:Functioning oncocytic islet-cell carcinoma. Report of a case with electron-microscopic and immunohistochemical confirmation. 300 44

The secretory response and immunoreactive heterogeneity of glucagon was investigated in a patient with glucagonoma syndrome. After glucose administration, abnormal insulin release accompanied by glucose intolerance were observed, whereas the high glucagon circulating levels were only partially blocked after glucose or somatostatin infusion. Chromatographic fractionation of plasma samples, before and after arginine administration showed that most of the immunoreactivity eluted as true glucagon. Furthermore, when aliquots of the tumor extracts were fractionated by column chromatography or by polyacrylamide gel electrophoresis, most of the immunoreactivity eluted in the 3,500 molecular weight peak. In contrast with previous reports, our results indicate that neoplasia A cells can also manufacture and release into the bloodstream great amounts of genuine glucagon rather than larger glucagon immunoreactive forms. In spite of such findings, in this patient neither diabetes nor hyperglycemia were present.
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PMID:Secretory response and immunochemical heterogeneity of glucagon in plasma and tumor extracts of a patient with glucagonoma. 300 53

Plasma immunoreactive glucagon (IRG) components were analyzed by gel filtration on either a Bio-Gel P-30 or a Sephadex G-150 column (1.0 X 68 cm) in a 47-year-old male with biopsy-proven malignant glucagonoma. Plasma samples were obtained before and after 20 courses of streptozotocin treatment as well as after administration of a somatostatin-derivative (SRIF-D, 0.38 mg, subcutaneous), regular insulin (0.2 U/kg, intravenous), and secretin (2 U/kg, intravenous). The fractions from the columns were assayed for IRG by simultaneous radioimmunoassay with C-terminal (Unger 30 K) and N-terminal (OAL 196) antibodies to glucagon. Four IRG components were observed. The largest had a molecular weight of approximately 150,000 daltons and cross-reacted much more strongly with the N-terminal antibody than with the C-terminal. The second IRG component appeared to be about 9000 daltons and cross-reacted more strongly with the N-terminal antibody. The third and major IRG component comprised 51.8% to 88.1% of the total IRG as measured with C-terminal antibody, corresponded in molecular weight to synthetic 3500 dalton glucagon, and reacted roughly equally with each of the two antibodies. The fourth IRG component cross-reacted only with N-terminal antibody and appeared to be smaller than 3500 daltons. The plasma IRG level decreased from 8829 pg/mL to 1421 pg/mL (averages of five consecutive determinations) after 20 courses of treatment with streptozotocin with significant clinical improvement. A marked (74%) but transient decrease in plasma IRG was observed after the SRIF-D injection, whereas secretion and insulin caused increases in plasma IRG level of 53% and 22%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunologic characterization of plasma glucagon components in a patient with malignant glucagonoma. 608 85

A 66 year old patient with diabetes had a necrolytic migratory erythema, weight loss and anaemia. Plasma immunoreactive glucagon (IRG) of 2465 pmoles/l (normal 35 +/- 5 SEM pmoles/l) suggested the existence of a glucagonoma which was confirmed by arteriography and subsequently removed by surgery. Although plasma IRG returned to normal, glucose tolerance and insulin secretion remained pathological. Plasma amino acid levels had been reduced but were corrected by surgery. Pancreatic polypeptide, however, 298 pmoles/l before was still 206 pmoles/l after the operation (normal 12-48 pmoles per litre). Column chromatography of plasma and tumor extracts showed quantitatively important IRG fractions with molecular weights above 9000 daltons, possibly precursors of glucagon. Beside a 50-fold IRG excess, the tumour concentrations of insulin and somatostatin were 4 to 150 times increased. By contrast, pancreatic polypeptide was present in normal amounts. Electron microscopic examination showed atypical A-cell granula and unusual abundance of mitochondria.
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PMID:In vitro and in vivo studies on glucagonoma tissue. 610 27

A family with multiple endocrine neoplasia type I (MEN-I) is described in which three members had A-cell pancreatic tumors. Two of these members had classic glucagonoma syndromes. The proband, a 62 year old woman, had a high (less than or equal to 9.2 ng/ml) basal plasma glucagon level, most of which eluted in the 3,500 dalton fraction. Plasma glucagon increased following the ingestion of mixed meals and arginine. Secretin, which, in the dog, has been reported to inhibit normal glucagon secretion, provoked a twofold increase in 3,500 dalton plasma glucagon concentration. Increased plasma glucagon in the proband was associated with mild hyperglycemia and insulin resistance. Somatostatin infusion suppressed peripheral glucagon and insulin levels, and increased blood glucose levels. The unique responses to secretin and somatostatin observed in this patient may be diagnostically important in syndromes of inappropriate or autonomous glucagon secretion.
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PMID:A familial glucagonoma syndrome: genetic, clinical and biochemical features. 611 77

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

Plasma responses of the major immunoreactive glucagon (IRG) components have been investigated in a case of glucagonoma syndrome. Fasting plasma IRG was 4155 pg/ml. Gel chromatography of plasma revealed that 66% of immunoreactivity was present as IRG9000, while IRG3500 accounted for an additional 26%. The appearance in peripheral plasma of these two glucagon fractions was examined after administration of a number of compounds. IRG levels were clearly elevated after arginine and tolbutamide. Both calcium and calcitonin induced a biphasic rise of IRG, the increase being slower after calcium administration. Somatostatin suppressed plasma IRG levels. All tests induced changes in both IRG3500 and IRG9000. In general, relative changes were more pronounced in IRG3500 than in IRG9000, while absolute changes were greater in IRG9000. The shape of the response curves of IRG3500 and IRG9000 was quite similar after arginine, calcium and somatostatin. After tolbutamide the IRG9000 response was delayed as compared to the IRG3500 component. During the latter part of the calcitonin infusion, IRG9000 remained elevated while IRG3500 was back at its starting level.
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PMID:The glucagonoma syndrome: stimulus-induced plasma responses of circulating glucagon components IRG9000 and IRG3500. 614 91

A further case of glucagonoma is reported, unusual features being the prolonged duration of cutaneous manifestations (12 years), and the absence of diabetes. Possible explanations for this anomaly: compensatory insulin or somatostatin secretion, production of a non functional glucagon, or low levels of circulating glucagon, are envisaged but without a formal response.
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PMID:[Glucagonoma without diabetes: a case report (author's transl)]. 626 28

The authors report a case of glucagonoma in a 52 years old man presenting a migratory necrolytic erythema. By conjugated means of arteriography and splenoportography with plasma glucagon assays the tumour was localized in the tail of the pancreas. Surgical excision was easy but hepatic metastases revealed the malignant nature of the tumor. This glucagonoma has been investigated by several approaches including electron microscopy, immunocytochemistry and radioimmunological techniques. The tumor contained scattered glucagon and pancreatic polypeptide immunoreactive cells; insuline, glucagon, somatostatin, pancreatic polypeptide, gastrin and VIP antisera gave negative results. Ultrastructurally, these cells showed atypical secretory granules different from A granules of the normal glucagon cell. Radio immunological determinations carried out after gel permeation chromatography of plasma revealed high molecular weight (4 000, 9 000, 14 000) immunoreactive glucagon peptides. They have been thought to be proglucagon forms which did not react with specific antiglucagon sera used in cytological studies. Reported data are consistent with the classification of this tumor in the category of glucagonoma with the "glucagonoma syndrome".
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PMID:[A human pancreatic glucagonoma, ultrastructural, immunocytochemical and radioimmunological investigations (author's transl)]. 627 65


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