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

Pancreas and gut hormones are involved in many endocrine and gastrointestinal diseases. Radioimmunoassays for these hormones have proved particularly valuable in diagnosis, localisation and control of treatment of endocrine tumours, of which many are mixed. An estimate based on ten years experience in a homogenous population of 5 million inhabitants (Denmark) suggests, that endocrine gut tumour-syndromes on an average appear with an incidence of 1 patient per year/syndrome/million. At present six different syndromes are known: 1) The insulinoma syndrome, 2) The Zollinger-Ellison syndrome.3) The Verner-Morrison syndrome. 4) The glucagonoma syndrome. 5) The somatostatinoma syndrome, and 6) the carcinoid syndrome. Accordingly diagnostically valuable RIAs for pancreas and gut hormones include those for insulin, gastrin, VIP, HPP, glucagon, somatostatin, and presumably also substance P. It is probably safe to predict that the need for gut and pancreas hormone RIAs within the next decade will increase greatly in order to assure proper management of tumours producing gastroentero-pancreatic hormones.
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PMID:Radioimmunoassay in diagnosis, localization and treatment of endocrine tumours in gut and pancreas. 22 84

The cellular composition of the pancreatic islets of juvenile diabetics was studied, using recently developed immunocytochemical methods. B-cells were identified only in juvenile diabetics with a disease of short duration. In chronic juvenile diabetics, the islets which are classically viewed as "atrophic", were shown to be composed of glucagon- and of somatostatin-cells. Another type of islets which commonly occurs in the pancreas of juvenile diabetics, i.e. the ribbon-like type first described by Cecil in 1911, appeared to be composed almost exclusively of "pancreatic polypeptide" (HPP)-cells. It is suggested that hyperplasia of the HPP-cells in the pancreas of juvenile diabetics results from an atypical type of islet regeneration induced by a severe and prolonged injury to the pancreatic endocrine tissue.
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PMID:Hyperplasia of "pancreatic polypeptide"-cells in the pancreas of juvenile diabetics. 32 79

Subtotal pancreatectomy specimens of seven infants with persistent hyperinsulinemic hypoglycemia were studied; all showed the characteristic light microscopic picture of nesidioblastosis. Specimens were studied by electron and conventional light microscopy and by light microscopic immunohistochemistry for insulin, glucagon, somatostatin, and HPP (human pancreatic polypeptide); double staining and quantitative methods were also used. Findings were compared with those in age-matched controls. In the hyperinsulinemic hypoglycemic infants, an increase in total endocrine cell volume was found; however, the typical features of nesidioblastosis were also found in the controls. In both groups, immunohistochemistry and electron microscopy suggested that some endocrine cells are capable of producing synchronously more than one hormone. Amphicrine ("composite" or "intermediate") cells with exocrine and endocrine differentiation were found in three hypoglycemic infants. Observations are discussed in relation to current concepts of embryogenesis of the gastroenteropancreative endocrine system. We conclude that nesidioblastosis, as defined anatomically cannot be considered as the morphologic basis of hyperinsulinemic hypoglycemia. The term "nesidiodysplasia" is suggested and includes increased, maldistributed, and malregulated or malprogrammed endocrine and amphicrine cells when associated with endocrine abnormality.
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PMID:Nesidiodysplasia and nesidioblastosis of infancy: structural and functional correlations with the syndrome of hyperinsulinemic hypoglycemia. 614 28

Subtotal pancreatectomy specimens from two adults with hyperinsulinemic hypoglycemia and one adult with watery diarrhea syndrome were investigated. All three specimens were originally diagnosed as "nesidioblastosis"; none had a neoplasm, and all patients were cured of their endocrine dysfunction by the surgical procedure. Tissue samples were studied by light microscopy and light microscopic immunohistochemistry for serotonin, ACTH, bombesin, calcitonin, gastrin, glucagon, insulin, HPP, somatostatin, and VIP. The results were compared with those obtained from the parallel study of ten adult pancreata obtained at autopsy from patients without pancreatic disease or endocrine dysfunction. The total endocrine cell mass was not notably greater in the pancreata from patients with endocrine dysfunction than in the controls. Both groups had an estimated 95% of the endocrine cell population organized in islets while the remaining 5% was irregularly dispersed amidst the exocrine ducts and acini. Findings more conspicuous in patients with endocrine dysfunction but not absent in the controls included: large islets, islets with irregular contours and ragged edges, and large individual islet cells with abundant cytoplasm and bizarre nuclei. Immunoreactivity for insulin, glucagon, and somatostatin was demonstrated in all cases; the ratio among these hormones in the patients with endocrine dysfunction and in the controls was similar. In the patients with hyperinsulinemic hypoglycemia, step sections sequentially stained for insulin and somatostatin showed a close topographic relationship between these cell types. In the patient with the watery diarrhea syndrome, VIP immunoreactive cells were easily identified admixed with exocrine components; they were only rarely seen within islets. We suggest that the hyperinsulinemic hypoglycemia in these adults was not due to simple quantitative abnormalities in total endocrine cell mass nor to its maldistribution nor to lack of topographic proximity between insulin and somatostatin cells. We speculate that the syndrome may be based on still unknown derangements of insulin secretion, release, and/or its degradation. In the case of the watery diarrhea syndrome, the readily identifiable VIP immunoreactive cells represent the emergence of a functional expression regarded as ectopic for the endocrine cells of the pancreas. We conclude that nesidioblastosis per se cannot be viewed as the structural basis of these endocrine dysfunctions since many of its features were present in control pancreata lacking any such association.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Adult nesidiodysplasia. 640 Jun 29

Endocrine cells are normal inhabitants of the anal canal. While numerous endocrine cells are distributed throughout anal ducts and crypts, few are dispersed in the anal transitional zone. All these cells were characterized as serotonin-storing cells, and this endocrine profile is quite distinctive from that of adjacent mucosae. Rectal epithelium contains serotonin, somatostatin, enteroglucagon, BPP and HPP immunoreactive cells; endocrine cells are lacking in the pectinal folds and perianal skin. It is suggested that this distinctive hormonal profile may be regarded as a specific marker of this anal territory. The same pattern is found in the fetal transitional lining of anal canal. Evidence of serotonin-storing cells in the transitional epithelium of anal glands and crypts and in the ATZ epithelium, reinforces the homology between these linings and urothelium. The presence of a similar fetal epithelium implies that ATZ epithelium in adults is not necessarily metaplastic. All derivatives of the cloaca may therefore share the same endocrine profile.
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PMID:Endocrine cells in the anal canal. 643 47

Fluoresceinated-avidin (FITC-avidin) was observed to bind specifically to a subset of pancreatic islet cells in sections of both human and rat pancreas. FITC-avidin binding was inhibited by excess unlabeled avidin, and by biotin, but not by glucagon, somatostatin, or insulin. Labeling of islets with anti-insulin, anti-glucagon, anti-somatostatin, and anti-human pancreatic polypeptide antibodies showed the avidin binding subset to correspond to islet cells identified by anti-glucagon antibody. Conversely, avidin reacted with no insulin, somatostatin, or cells containing HPP. We conclude that avidin localizes specifically to A-islet cells. Binding may be to a biotin-containing enzyme within the A-cells, but the precise molecular site of binding is currently unidentified.
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PMID:Selective binding of fluoresceinated-avidin to A-cells of sectioned pancreas. 675 27

The regional distribution and frequency of pancreatic endocrine cells in ddY mice were studied by an immunohistochemical (peroxidase anti-peroxidase; PAP) method using four types of specific antisera against insulin, glucagon, somatostatin and human pancreatic polypeptide (hPP). In the pancreatic islets, most of insulin-immunoreactive (IR) cells were located in the central portion. Most of glucagon- and somatostatin-IR cells were observed in peripheral regions although a somewhat smaller number of cells were also located in the central regions. HPP-IR cells were randomly distributed throughout the entire islets. In the exocrine pancreas, insulin-, glucagon-, somatostatin- and hPP-IR cells were detected; they occurred mainly among the exocrine parenchyma as solitary cells. Cell clusters consisted of only insulin- or only glucagon-IR cells and were distributed in the pancreas parenchyma as small islets. In addition, insulin- and glucagon-IR cells were also demonstrated in the pancreatic duct regions. Insulin-IR cells were located in the epithelium and sub-epithelial connective tissue regions as solitary cells and/or clusters (3-4 cells), and glucagon-IR cells were mainly located in the epithelium as solitary cells. Overall, there were 63.89+/-5.39% insulin-, 26.52+/-3.55% glucagon-, 7.25+/-2.83% somatostatin- and 1.90+/-0.58% hPP-IR cells. In conclusion, some strain-dependent characteristic distributional patterns of pancreatic endocrine cells were found in the ddY mouse.
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PMID:Distribution and frequency of endocrine cells in the pancreas of the ddY mouse: an immunohistochemical study. 1596 40