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 distribution and morphology of intestinal endocrine cells was investigated in the mucosa of pelvic ileal reservoirs using immunocytochemical methods. Endoscopic biopsies were obtained from 15 patients after the construction of a modified J-pouch. The mucosa of the reservoir showed a variable degree of colonic metaplasia in all cases. No relevant quantitative variations of gut endocrine cells were detected, as revealed by immunostaining for the general marker, chromogranin, compared with normal ileal mucosa. Immunostaining for different peptide-containing cells resulted in normal number and morphology of serotonin, enteroglucagon, peptide tyrosine-tyrosine, and somatostatin-containing cells. Neurotensin cells were less numerous than in normal mucosa. The role played by gastrointestinal hormones in the adaptive response of the intestine to pouch construction is, presently, unclear. Further studies involving measurements of fasting and meal-stimulated levels of gut hormones in pouch patients might clarify this aspect.
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PMID:Immunocytochemical study of endocrine cells in pelvic ileal reservoirs. 197 12

Somatostatin and its longer-acting analog, octreotide acetate, can be used effectively for the treatment of nonendocrine gastrointestinal disorders. Octreotide has been shown to decrease pancreatic fistula output by suppressing exocrine pancreatic function. We believe that octreotide acetate may be useful to prophylaxis against the development of pancreatic fistulas following pancreatic resection and may reduce the enzymatic and volume output of established pancreatic fistulas. We also have shown that administration of octreotide acetate 2 hours before a high carbohydrate test meal reduces gut peptide levels, which increase following meal ingestion in patients with the dumping syndrome. Reduction of circulating peptides in these patients may slow gut motility and improve glucose regulation, thus, providing relief of postvagotomy dumping symptoms.
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PMID:Treatment of nonendocrine gastrointestinal disorders with octreotide acetate. 197 12

Somatostatin-14 and somatostatin-28 are biologically active peptides derived from the posttranslational cleavage of prosomatostatin. Because both peptides are found in variable concentrations in the gastrointestinal (GI) tract and pancreas, it has been contended that somatostatin-28 is either an intermediate in the processing to somatostatin-14 or a terminal product derived from prosomatostatin. To address this question, two antisera were used to recognize epitopes in two regions of somatostatin-14; one with high specificity for somatostatin-14 and the other interacting with prosomatostatin, somatostatin-28, and somatostatin-14. Distribution of these peptides was measured in extracts of pancreas and mucosa and submucosa/muscularis from the rat and human GI mucosal biopsies; the antisera were used to immunostain cells in these tissues. Extracts of human and rat intestinal mucosa contained both somatostatin-28 and somatostatin-14. By immunocytochemistry, D cells in stomach and pancreas and neural processes in the intestine, extending into the mucosal villi adjacent to endocrine cells, stained with both antisera indicating the presence of somatostatin-14, prosomatostatin, and possibly somatostatin-28. In contrast, endocrine cells in the gut reacting with antisera against somatostatin-28 did not immunostain with somatostatin-14-specific antisera. Thus, these data suggest that somatostatin-28 is the terminal peptide processed from prosomatostatin in intestinal mucosal cells, whereas somatostatin-14 is the major final product in gastric and pancreatic D cells and neurons. The localization of somatostatin-28 and somatostatin-14 in different cells in the pancreas and GI tract implies that they serve different functions.
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PMID:Distribution of somatostatin-14 and somatostatin-28 gastrointestinal-pancreatic cells of rats and humans. 197 60

The aganglionic intestine in Hirschsprung's disease displays a severe neuronal derangement. The changes are particularly evident in the muscular innervation. In the gut the endocrine cells are among the cells known to be influenced by neurons. We have, therefore, examined the endocrine cells in ganglionic and aganglionic intestine using immunocytochemistry and immunochemistry. The endocrine cells were studied using antibodies against the neuroendocrine marker chromogranin A, the amine serotonin and the hormonal peptides somatostatin, glucagon/glicentin and peptide YY (PYY), thus covering virtually all endocrine cell types known to occur in this region. The PYY concentration in the mucosal layer was measured by radioimmunoassay. In ganglionic as well as in aganglionic intestine large populations of cells storing chromogranin A, serotonin, glucagon and PYY and a smaller population of somatostatin cells were seen. There was an increase in the density of these cells in the aganglionic intestine compared with ganglionic. The data indicate that the endocrine cell populations in the intestinal wall can be maintained despite severe derangements of the nerve supply.
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PMID:Intestinal endocrine cells in Hirschsprung's disease. No reduction in density in aganglionic compared with ganglionic segment. 197 32

Epidermal Growth Factor (EGF)-containing cells have been found in Brunner's glands in the same area where several regulatory peptides are released. The present study was aimed at testing the release and the regulation of EGF secretion from cultured duodenal biopsies obtained from healthy individuals by gastroscopy. The effects and the interaction of VIP and somatostatin on the hormone release were studied. Duodenal biopsies were cultured at 37 degrees C in Mc Coy's buffer, gassed with 95% O2 and 5% CO2. After 30 min, the culture medium was decanted for the measurement of the hormones by RIA. To measure the protein content, the tissue was then homogenized; EGF detected in the culture was 11.5 ng/mg protein. The addition of VIP in the medium increased EGF mean levels to 21.6 ng/mg protein (P less than 0.01). The biopsies thus obtained were cultured with anti-somatostatin antibodies to evaluate the influence of endogenous somatostatin on EGF secretion. The inclusion of anti-somatostatin antibodies increased the EGF levels to 41.2 ng/mg protein (P less than 0.01). The combined addition of anti-somatostatin antibodies and VIP in the culture caused a mean EGF increase significantly higher than the values obtained separately by VIP and somatostatin (P less than 0.01). In conclusion, we can suggest a triangular interaction model of EGF release, where the somatostatin seems to be the negative monitor of over-secreted VIP and EGF from the gut.
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PMID:Role of vasoactive intestinal polypeptide (VIP) and endogenous somatostatin on the secretion of epidermal growth factor (EGF): studies on duodenal tissue cultures. 197 88

The role of vagus nerve for release of gastrin, secretin and somatostatin in dogs was studied. Bilateral cervical vagotomy and electric vagal stimulation (25 V 0.5 msec 10 Hz) were performed and blood levels of gut hormones were measured. After vagotomy, blood levels of gastrin, secretin and somatostatin did not change. The electric vagal stimulation elevated blood level of gastrin. Atropine and hexamethonium inhibited the elevation. The electric vagal stimulation did not change blood levels of secretin and somatostatin. In conclusion, vagal stimulation releases gastrin into blood circulation depending on the cholinergic mechanism.
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PMID:[Role of vagus nerve for release of gut hormones]. 197 45

Food intake results in a variety of responses, with the autonomic nervous system playing an important role in maintaining cardiovascular homeostasis. In patients with autonomic failure, who have severe sympathetic impairment, food substantially lowers blood pressure even in the supine position. This is related to a marked increase in splanchnic blood flow, without compensatory changes in the rest of the circulation. Of the food components, glucose causes similar effects to food, while an isosmotic, isocaloric load of the inert carbohydrate, xylose, causes only a small fall in blood pressure. Lipid causes a small, short-lived fall in blood pressure and protein causes minimal change. Insulin appears to contribute to the fall in blood pressure, as bolus injections of insulin (even before ensuing hypoglycaemia), or insulin infusions (with an euglycaemic clamp), when given intravenously lower blood pressure. Other vasodilatatory gut peptides released by food may also play a role. The somatostatin analogue, Octreotide (SMS 201-995), which inhibits the release of a range of peptides, prevents both glucose and food-induced hypotension. Studies of the mechanisms responsible for post-prandial hypotension in autonomic failure continue to provide insight into the relationship between food intake and the hormonal, peptidergic and neural responses which affect the cardiovascular system.
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PMID:Effect of food intake on cardiovascular control in patients with impaired autonomic function. 197 48

The effects of parasitic infection on plasma and tissue content of immunoreactive somatostatin (SRIF) were studied in 4-mo old male calves inoculated with the protozoan Sarcocystis cruzi. Because feed intake significantly decreased (70%) in infected calves around day 28 postinfection (pi), concomitant with the asexual replication of S. cruzi and outward expression of clinical signs, the relative contributions of infection and associated reduction in nutrition on plasma SRIF were evaluated. Treatment groups were: noninfected ad libitum fed (C), infected (250,000 S. cruzi oocysts per os) ad libitum fed (I) and noninfected calves pairfed to the level of intake of each infected calf (PF). Mean plasma concentrations of SRIF (pg/ml) on day 30 pi were: C, 224 +/- 22; I, 742 +/- 150; PF, 246 +/- 31 (effect of infection P less than .05). In another study, SRIF was measured in plasma and in pancreatic, duodenal, jejunal and ileal tissue extracts from normal and S. cruzi infected calves. Plasma and tissue samples were collected on day 42 pi. Mean plasma SRIF were 2.5 times higher in infected than control calves. Plasma insulin and insulin-like growth factor 1 was lower in infected v control calves (P less than .02). Plasma glucagon was similar between groups. Duodenal (P less than .05) and jejunal (P less than .02) SRIF content was higher in infected than control calves. Chromatography of tissue extracts on Sephadex G-50 revealed that the increase in SRIF was accounted for, in part, by molecular forms larger than cyclic SRIF-14. Data suggest that peripheral SRIF is increased in calves during S. cruzi infection. The increase in SRIF is not solely related to plane of nutrition. Altered levels of gut SRIF(s) may be associated with perturbed metabolic regulation in parasitized animals through direct effects on the gut.
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PMID:Plasma and tissue concentrations and molecular forms of somatostatin in calves infected with Sarcocystis cruzi. 197 66

The present study is an investigation of the effects of 12- to 96-hours' starvation and 96-hours' starvation plus 48-hours' refeeding on both somatostatin-like immunoreactivity (SLI) and cytosolic somatostatin binding sites in rabbit small intestinal mucosa. The SLI concentration increased after 24 h in duodenal and jejunal mucosa, but not in ileal mucosa, and reached its highest value after 96 h of fasting. The number of specific high and low-affinity somatostatin binding sites, but not their affinity, decreased with the duration of fasting in the same gut segments, refeeding of fasted animals resulted in a return to normal control values for small intestine mucosal SLI and somatostatin binding.
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PMID:Somatostatin content and binding in small intestinal mucosa from fed, fasted, and refed rabbits. 198 Mar 31

The somatostatin (SS), the SS mRNA, and the SS receptor contents were measured and compared in 25 human meningiomas. The SS tissue content, measured with radioimmunoassay, amounted to 2.89 +/- 0.82 pg/mg tissue (mean +/- SEM). The SS mRNA levels visualized by in situ hybridization using a 32P-labeled synthetic oligonucleotide probe were undetectable in all cases. SS receptors were measured with autoradiography using the octapeptide SS analogue 125I-204-090 as radioligand and were found to be present in high density in all meningiomas. For comparison, three SS-producing tumors, i.e., two human medullary thyroid carcinomas and one neuroendocrine gut tumor, were shown to have a high level of immunoreactive tissue SS, reaching, respectively, 2807, 401, and 22 pg/mg tissue, as well as moderate to high levels of SS mRNA detected with in situ hybridization. It can be concluded that meningioma tissue is not synthesizing significant amounts of SS in situ and that the low amount of tissue SS found in these tumors is likely to be due to SS transported there from a distant source, via blood, cerebrospinal fluid, or axons from nerve fibers terminating in this tissue. The high number of SS receptors found in meningiomas is therefore unlikely to be regulated by an autocrine SS production from the meningioma tissue itself but rather from another, unknown distant SS source.
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PMID:Lack of evidence for autocrine feedback regulation by somatostatin in somatostatin receptor-containing meningiomas. 198 Jun 1


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