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)

A hybridoma monoclonal antibody against human pepsinogen I was used to develop an enzyme-linked immunosorbent assay for pepsinogen I in serum. In the two-step competitive procedure using antimouse immunoglobulin F(ab')2 fragment coupled to alkaline phosphatase, the measurable assay range was 8-256 micrograms/l. No cross-reactivity with rat pepsinogen 1, human pepsinogen II, gastrin I, bombesin, somatostatin and peptide YY was shown. However, there was slight cross-reactivity (0.09%) with porcine pepsinogen. The coefficients of variation within and between series were 7.6% and 13.0%. This enzyme-linked immunosorbent assay for serum pepsinogen I correlated positively with radioimmunoassay (r = 0.87, n = 92). The concentration range of serum pepsinogen I in 354 healthy controls was 15-100 micrograms/l with a lognormal distribution. Serum pepsinogen I levels were significantly higher in the subjects who developed active duodenal ulcer or active gastric ulcer, but significantly lower in those who had gastric cancer, than in control subjects.
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PMID:Enzyme-linked immunosorbent assay of serum pepsinogen I. 380 50

Six healthy young males were studied with an intravenous infusion of saline for 1 h, followed by somatostatin, 100 microgram/h, for 2 h, and thereafter by another 2 h with saline infusion. Gastric H+ and pepsin outputs were determined in 30-min periods throughout the study. Blood was drawn at regular intervals, and blood glucose was determined by a hexokinase method. PG I and gastrin in serum were determined by radioimmunoassay methods. Gastric H+ and pepsin outputs were markedly reduced during the somatostatin infusion and the first 30-min period after cessation of the somatostatin infusion. In the subsequent 60-min period gastric pepsin secretion increased significantly as compared with the basal period, whereas the gastric H+ output only increased non-significantly. Mean serum PG I increased during the somatostatin infusion and remained elevated throughout the study. The rise in serum PG I was marked in five and only marginal in the sixth person. Serum gastrin fell during the somatostation infusion and returned to the basal level thereafter. Blood glucose, on the other hand, fell only during the first 90 min of somatostatin infusion, and then climbed to the basal level, where it stayed for the remaining part of the study. The present results suggest that the pepsinogen synthesis is unaffected by somatostatin, and that serum PG I seems to reflect the amount of pepsinogens stored in the gastric mucosa.
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PMID:The effect of somatostatin on serum group I pepsinogens (PG I), serum gastrin, and gastric H+ and pepsin secretion in man. 610 88

Proliferating cells in the gastric mucosal epithelium were successfully enriched by counterflow elutriation in a medium-sized cell fraction. When inoculated on culture plates coated with E-C-L cell attachment matrix, these cells differentiated into mucus-producing cells after reaching confluence. Northern blot analysis did not detect any transcript of the proton pump, histidine decarboxylase, somatostatin, or pepsinogen I, indicating the absence of parietal, ECL, D, and chief cells in the confluent monolayer. These mucus-producing cell monolayers that respond to various growth factors may be a suitable model with which to investigate the function of gastric mucus cells in vitro.
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PMID:Establishment of primary epithelial cell culture from elutriated rat gastric mucosal cells. 777 41

Radioimmunoassay and immunomorphological methods were used in the study of pepsinogen 1, basal and food-stimulated gastrin and somatostatin blood levels, the number of gastroduodenal G- and D-cells as well as gastric secretion during routine-dose treatment with gastrozepin and ranisan of 45 gastroduodenal ulcer patients versus 15 controls. The patients were divided into 2 types according to blood gastrin levels and the number of pyloric G-cells: with hypergastrinemia and/or hyperplasia of the G-cells, with normogastrinemia and normal number of G-cells. A course treatment with gastrozepin of type 1 patients brought about normalization of serum gastrin and the number of the G-cells with elevation of blood somatostatin levels. In patients of type 2 the above parameters did not change. The same picture in them remained after ranisan treatment, though they developed hypergastrinemia. In patients of type 1 after ranisan treatment the above parameters did not change. The data obtained demonstrate once more heterogeneity of duodenal ulcer.
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PMID:[Levels of gastrin and somatostatin in blood and gastroduodenal gastrin and somatostatin cells in the differentiation of treatment of patients with duodenal ulcer]. 785 18

Inhibition both in vivo and in vitro of pepsinogen secretion by somatostatin (SS) and the histological demonstration that fundic D-cells contain long cytoplasmic processes extending to chief cells suggest a possible direct effect of SS on chief cell function. The aim of the present study was to determine whether SS interacts directly with receptors on isolated gastric chief cells and, if so, how SS alters cell function. Binding of 125I-[Tyr11]SS14 to chief cells was saturable, time and temperature dependent, and was inhibited by both SS14 (Ki 1.6 nM) and SS28 (Ki 5.2 nM). SMS-201-995 was 1,300-fold less potent than SS14. Calcium-mobilizing secretagogues reduced binding of 125I-[Tyr11]SS14 with efficacies of cholecystokinin octapeptide (CCK-8) > carbachol > gastrin. Adenosine 3',5'-cyclic monophosphate (cAMP)-activating secretagogues also inhibited binding with efficacies of secretin > vasoactive intestinal polypeptide (VIP). 12-O-tetradecanoylphorbol 13-acetate (TPA) or A-23187 also decreased binding. Analyses demonstrated that CCK-8 and TPA were decreasing the affinity of SS receptors for 125I-[Tyr11]SS14 without affecting their binding capacity. Both SS14 and SS28 at a maximally effective concentration inhibited cAMP production caused by VIP or secretin (20-30%) but did not alter cytosolic calcium ([Ca2+]i), inositol phosphates, or pepsinogen release. We conclude that chief cells possess SS receptors with a high affinity for both SS14 and SS28 but low affinity for SMS-201-995 and thus resemble the SSB receptors described in the rat cerebral cortex. Although occupation of these receptors by SS has no effect on pepsinogen release induced by secretagogues acting through either the calcium or the cAMP pathway, SS receptor occupation is regulated by agents activating phospholipase C, adenylate cyclase, protein kinase C, and [Ca2]i.
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PMID:Chief cells possess somatostatin receptors regulated by secretagogues acting through the calcium or cAMP pathway. 791 Dec 77

Antral gastrin cell hyperfunction (AGCH) is a rare syndrome characterized by persistent hypergastrinemia and important peptic symptoms in the absence of a gastrin-producing tumor. The pathogenesis of AGCH is still unknown and debated. Helicobacter pylori (Hp) infection has been reported as a possible cause of sustained hypergastrinemia. To assess the relevance of Hp infection in pediatric AGCH patients, Hp status, G cell function, acid secretion, and antral G and D cell populations were investigated in six children presenting with gastrointestinal bleeding of unknown origin, sideropenic anemia, and variable abdominal symptoms. All patients had moderate high basal gastrinemia with abnormally increased peak values after meals and elevated values of basal acid output (BAO), maximal acid output (MAO), and pentagastrin-stimulated acid output (PAO). Circulating pepsinogen I was also significantly increased. Three children had Hp infection, as assessed by enzyme-linked immunosorbent assay, urease test, and histology. Endoscopy showed duodenal erosions in three children, with ulcer in two Hp-positive cases. At histology, moderate gastritis was observed only in the three Hp-positive cases. In all patients, quantitative assessment of antral gastrin and somatostatin cells gave significantly elevated G cell counts; D cells were at the lower reference limit and the G/D cell ratio was significantly elevated. These data indicated a diagnosis of AGCH, possibly due to the elevated G/D cell ratio, and suggest HP infection as an overlapping factor complicating the clinical picture in some cases.
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PMID:Helicobacter pylori infection in children with antral gastrin cell hyperfunction. 791 67

We examined the inhibitory effect of somatostatin on pepsinogen secretion using isolated rat gastric chief cells. Secretin and forskolin significantly increased not only pepsinogen secretion from chief cells but also cellular cAMP accumulation in a dose-dependent fashion. Somatostatin significantly inhibited secretin- and forskolin-induced pepsinogen secretion and secretin-induced cellular cAMP accumulation. However, forskolin-induced cellular cAMP accumulation was not inhibited by somatostatin. The inhibitory effect of somatostatin on secretin-induced pepsinogen secretion was abolished by pretreatment with pertussis toxin, but inhibition of forskolin-, carbachol- and cholecystokinin octapeptide-induced pepsinogen secretion was not. These results suggest that somatostatin inhibits pepsinogen secretion in two ways, one is closely related to the pertussis toxin-sensitive G-protein and the other is not determined.
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PMID:Inhibitory action of somatostatin on cAMP dependent pepsinogen secretion from rat gastric chief cells: involvement of pertussis toxin-sensitive G-protein. 791 4

Cholecystokinin stimulates pancreatic zymogen secretion by binding with high affinity to a receptor on the pancreatic acinar cell. This receptor has been cloned and shown to be a CCK-A subtype. CCK also stimulates pepsinogen secretion from the gastric chief cell with high affinity. Using polymerase chain reaction with primers from the known sequence of the rat pancreatic CCK-A receptor cDNA, we prepared a 600 bp product from rat and rabbit stomach cDNA. From Southern analysis these represented a fragment of a gastric CCK-A receptor. PCR was then used to amplify a rabbit lambda ZAP II gastric epithelial cDNA library with the same primers, and the product was identified by sequencing as representing a CCK-A receptor fragment. When this PCR product was used to screen the library, ten positive clones were identified in a screening of 4.10(5) plaques, and several of these were sequenced. All had essentially the same sequence contained within 2 of these clones consisted of 427 amino acids and was 92% homologous (87% identity) to the known rat pancreatic CCK-A sequence but only 43% homologous to the gastric CCK-B sequence. The cDNA was subcloned into a pcDNA1 expression vector and transiently expressed in the human embryonic kidney cell line, HK 293. The responses of intracellular Ca2+ in these transfected cells to CCK and gastrin were monitored using video imaging. On the average 40% of the cells responded to CCK-8 by a transient elevation of [Ca2+]i followed by a steady state plateau. CCK was a high and gastrin a low affinity ligand for this signal, corresponding to the actions of these ligands on pepsinogen secretion from chief cells and somatostatin release from D cells. Hence from sequence and second messenger responses, the clone represents the CCK-A receptor presumably responsible for pepsinogen secretion by gastric chief cells and somatostatin release from gastric D cells.
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PMID:Cloning and expression of the rabbit gastric CCK-A receptor. 791 28

Gastric chief cells were isolated from the rat stomach in an attempt to identify those involved in the mechanism of action of somatostatin on pepsinogen secretion. The effects of several kinds of secretagogues on cytosolic free Ca2+ concentration ([Ca2+]i) were examined in the rat chief cells. Carbachol and cholecystokinin octapeptide (CCK-8) markedly induced [Ca2+]i increase, while histamine, gastrin I and secretin did not. Carbachol and CCK-8 also stimulated pepsinogen secretion. A similar dose-response relationship was seen in carbachol- and CCK-8-induced [Ca2+]i increase and pepsinogen secretion. Somatostatin did not inhibit carbachol- or CCK-8-induced [Ca2+]i increase, but did inhibit carbachol- and CCK-8-induced pepsinogen secretion by 30 and 50%, respectively.
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PMID:Somatostatin inhibits pepsinogen secretion without influencing cytosolic free Ca2+ increase induced by carbachol and cholecystokinin octapeptide in rat chief cells. 810 77

Nineteen different antisera raised against mammalian hormones were used to identify the occurrence and distribution of endocrine cells in the gut of grass carp (Ctenopharyngodon idellus). Positive reactions were obtained in gut epithelium with antisera gastrin, glucagon, gastric inhibitory peptide, leucine enkephalin, substance P, and bovine pancreatic polypeptide. No immunoreactive product was formed using antisera against somatostatin, 5-hydroxytryptamine, insulin, avian pancreatic polypeptide, motilin, cholecystokinin, secretin, neurotensin, vasoactive intestinal polypeptide, bombesin, neuron-specific enolase, prochymosin, and pepsinogen. The exact distribution mapping of six kinds of immunoreactive endocrine cells throughout the gut of grass carp (C. idellus) is presented. The morphological characteristics of immunoreactive endocrine cells is described. Their distribution characteristics and possible modes of secretion and function are discussed. Finally, the possible relationship between the transplantation of these cells in the gastro-entero-pancreatic endocrine system is discussed.
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PMID:An immunocytochemical study of endocrine cells in the gut of a stomachless teleost fish, grass carp, Cyprinidae. 816 83


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