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)

Grimelius reaction and immunohistochemical PAP method were used to study endocrine cells producing gastrin (G-cells), somatostatin (D-cells) and gamma-endorphin (GER-cells) in gastric and duodenal mucosa of 95 males with atrophic gastritis with intestinal and pyloric metaplasia. The number of cells was counted per 1 mm2 of the mucosa. In the cases of marked intestinal metaplasia the number of G-, GER- and especially D-cells in the pyloric region non-metaplastic epithelium decreases and is approaching to its number in the duodenum of the control group. In the foci of marked pyloric metaplasia of gastric corpus the number of G- and GER-cells is almost the same as in the zones of gastric metaplasia of duodenum, and is approximating their number in the pyloric region of controls, thus allowing the designation of pyloric metaplasia as a complete one.
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PMID:[Gastrointestinal endocrine cells in metaplasia of the gastric mucosa and duodenum]. 243 May 53

Smooth muscle specimens were taken from the lower esophageal sphincter of patients suffering from achalasia or hiatus hernia with gastro-esophageal reflux. The specimens were analysed for neurohormonal peptides using immunochemistry and immunocytochemistry. Control specimens were obtained from patients subjected to esophageal resection because of esophageal cancer. The concentration of vasoactive intestinal polypeptide (VIP) was higher and the VIP nerve supply greater in patients with hiatus hernia than in control patients. The VIP nerve supply and the content of this peptide was lower in patients with achalasia than in controls. The same tendency was observed for substance P and enkephalin although the changes in their concentrations were not statistically significant. Enkephalin fibers were few, both in specimens from control patients and from patients with hiatus hernia; they could not be detected in specimens from patients with achalasia. Never fibers containing somatostatin or gastrin/cholecystokinin could not be detected in any of the groups and somatostatin and gastrin/cholecystokinin could not be measured in extracts of the lower esophageal sphincter. We propose that changes in the concentration of neuropeptides may at least contribute to manifestations of achalasia and of decreased lower esophageal sphincter pressure and gastro-esophageal reflux.
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PMID:Regulatory peptides in the lower esophageal sphincter of man. 258 Dec 86

The impact of overnight intravenous lipid emulsion (ILE) infusion on upper gastrointestinal tract physiology was assessed in 10 healthy volunteers. No changes in lower esophageal sphincter pressure (before infusion: 28 +/- 4 mm Hg; after infusion 20.5 +/- 3; p:NS), plasma concentrations of gastrointestinal hormones (gastrin: preprandial before/after lipids: 14 +/- 2.1/13 +/- 1.4 pM; postprandial before/after lipids: 28 +/- 2.7/30 +/- 3.4 pM, CCK: preprandial before/after lipids: 69 +/- 10/64 +/- 10 pM; postprandial before/after lipids: 96 +/- 11/95 +/- 12 pM; neurotensin: levels less than 6 pM in all samples; somatostatin levels undetectable in all samples) nor on pathologic gastroesophageal reflux episodes (% of time of pH less than 4, before/after lipids: 0.6 +/- 0.4/0.15 +/- 0.09), were found (p = NS). In contrast, technetium gastric emptying studies showed a significant delay when comparing pre- and post-lipid infusion values (37 +/- 4/54 +/- 4%) (p greater than 0.005). The mechanism of this effect remains unexplained.
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PMID:Intravenous fat emulsion (intralipid) delays gastric emptying, but does not cause gastroesophageal reflux in healthy volunteers. 276 Oct 66

The oesophageal pH was recorded for 3 h after a test-meal in 27 healthy control subjects (group I), 40 patients with alcoholic cirrhosis (group II), and 22 patients with a normal liver and symptoms of gastro-oesophageal reflux (control refluxers). Gastro-oesophageal reflux was observed in 10 of the cirrhotic patients. Marked reflux episodes lasted longer in cirrhotic refluxers than in control refluxers (P less than 0.05). The frequency of ascites, bleeding from ruptured oesophageal varices, peripheral neuropathy and hepatic encephalopathy were not significantly different according to presence or absence of reflux. Plasma concentrations of gastrin, somatostatin, motilin and vasoactive intestinal peptide (VIP) were measured in groups I and II. Fasting plasma motilin levels, and the release of motilin and of VIP after the meal were higher in group II than in group I. Basal levels and post-prandial profiles of the four peptides tested did not differ between cirrhotics with or without gastro-oesophageal reflux. We conclude that in patients with alcoholic cirrhosis: gastro-oesophageal reflux is frequent (25%) and characterized by prolonged reflux episodes; reflux is not correlated with the degree of liver failure and plays no significant role in the rupture of oesophageal varices; and raised plasma motilin and VIP levels cannot account for the high incidence of reflux in cirrhotics.
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PMID:Gastro-oesophageal reflux and alcoholic cirrhosis. A reappraisal. 288 50

Acidification of the gastric cardia has been shown to increase lower esophageal sphincter pressure (LESP). The mechanism by which this phenomenon occurs remains unknown. This study was undertaken to examine the effect and mechanism of action of proximal gastric acidification on LESP in the dog model. In long-term studies, acidification resulted in a significant increase in mean LESP (23.2 cm H2O). Pretreatment with either topical lidocaine or subcutaneous atropine blocked the sphincteric response to acidification. Neither truncal vagotomy and pyloroplasty, proximal gastric vagotomy, antral vagotomy and pyloroplasty, nor circumferential gastric myotomy significantly altered the sphincteric response to acid. Pretreatment with 6-hydroxydopamine or somatostatin also failed to alter the increase in LESP in response to acid. In short-term studies, after gastric transection 5 cm distal to the gastroesophageal junction, acidification of a vagally innervated distal gastric pouch produced a slight decrease in LESP, whereas acidification of the proximal (orad) section of gastric mucosa still resulted in a significant increase in LESP. These studies suggest that the increase in LESP observed with acidification of the gastric cardia is a local mechanism mediated by an intrinsic neural pathway dependent on cholinergic neurotransmission. This phenomenon of local reflex excitation may be another contributing mechanism to the barrier against gastroesophageal reflux.
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PMID:The mechanism of acid-induced increases in canine lower esophageal sphincter pressure. 292 55

Three types of endocrine cells (G cells producing gastrin-17, D cells producing somatostatin, and GER cells containing endorphine) in the mucous membrane of the stomach antrum from 14 patients with duodenal ulcer and 10 healthy persons were studied. Biopsies were fixed in a modified Bowen solution and imbedded into paraffin. The slides were stained by Grimelins' method and immunohistochemically with the use of the peroxidase-antiperoxidase method. The number of cells per 1 mm2 of the mucous membrane was counted. Patients with ulcer have shown the increased number of G and GER cells and decreased number of D cells. Besides, pronounced G cell hyperplasia with a relative decrease of GER cells and a marked decrease of Grimelins-positive cells (as compared to other patients with duodenal ulcer) were observed in 3 out of 14 ulcer patients. The authors conclude that the alteration of the balance between antagonistic hormone effects results in the hypersecretory syndrome that plays the main role in the pathogenesis of duodenal ulcer.
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PMID:[Gastric endocrine cells containing endorphin, gastrin and somatostatin in duodenal ulcer]. 614 55

While pancreatic metaplasia has been observed in gastric mucosa of patients with chronic gastritis, it has not been described in ectopic gastric mucosa. We have identified focal clusters of cells resembling pancreatic acinar cells (CPACs) in 11 of 350 biopsies of Barrett's mucosa from 120 patients with Barrett's esophagus enrolled in a clinical efficacy trial of omeprazole versus ranitidine for treatment of gastroesophageal reflux disease. Three additional cases from our surgical files were also studied. Immunoreactivity for trypsin and chymotrypsin was present in the CPACs of all 14 cases, while stains for alpha-amylase and lipase were each positive in 12 of 13. A few cells in the CPACs were also positive for chomogranins (12 of 13 cases), serotonin (seven of 13 cases), somatostatin (three of 12), gastrin (four of 11), and pancreatic polypeptide (two of 13). No staining was seen for insulin or glucagon. Ultrastructural studies performed in one case showed features of pancreatic exocrine and endocrine (PP-type) cells in cells within CPACs. These results collectively indicate that the CPACs are aggregates of true pancreatic acinar cells admixed with a few endocrine cells. This pancreatic parenchyma in Barrett's mucosa is most likely of metaplastic origin and could be derived from the transitional zone cells or from pluripotent stem cells in the esophageal mucosa or from metaplasia of mucus cells. While the development of pancreatic metaplasia in Barrett's esophagus appears to be unrelated to drug therapy, the clinical relevance of this distinctive histological finding needs further investigation.
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PMID:Pancreatic metaplasia in Barrett's esophagus. An immunohistochemical study. 757 75

Transient lower esophageal sphincter relaxations (TLESRs) are the major mechanism of reflux in patients with gastroesophageal reflux disease. They are therefore attractive targets for pharmacotherapy. During the past 5 years, there has been a burgeoning interest in the neural pathways that control these events and in the pharmacologic receptors involved in these pathways. Several agents have been shown to reduce the rate of TLESRs, including cholecystokinin-A antagonists, anticholinergic agents, nitric oxide synthase inhibitors, morphine, somatostatin, serotonin type 3-receptor antagonists, and gamma-aminobutyric acid-B (GABA(B)) agonists. Their predominant site of action appears to be on either the afferent pathways and/or the central integrative mechanisms within the dorsal vagal complex in the brainstem. Most of the agents tested are unsuitable for clinical use either because of side effects or because of the lack of an orally effective formulation. The most promising agents identified to date are the GABA(B) agonists. Baclofen, the prototype GABA(B) agonist, inhibits the rate of TLESRs by more than 50%. Control of TLESRs is a major new approach to the treatment of reflux disease. It is likely to be applicable to the majority of patients, particularly those without macroscopic mucosal lesions or only mild erosive disease. Further development of more effective agents will depend both on a better understanding of the neural pathways and receptors involved in the control of TLESRs, as well as on investigation of other novel agents. At present, inhibition of TLESRs is at the threshold of transition from concept to practical use. Whether it makes the final leap into the mainstream of therapy will depend on the development of new, novel, and well-targeted pharmacologic agents.
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PMID:Systemic pharmacomodulation of transient lower esophageal sphincter relaxations. 1174 47

We systematically reviewed the literature on gastroesophageal reflux disease (GERD) related to Helicobacter pylori therapy, and classified the GERD according to various aspects. Preexisting GERD is active GERD before H. pylori therapy, and a substantial proportion of the GERD patients improve after successful H. pylori therapy. If the GERD does not persist or recur after cessation of acid-suppressive therapy combined with H. pylori therapy, it may have been cured (cured GERD). If it recurs, it may have been masked by acid-suppressive therapy and unmasked with cessation of the therapy (pharmacologically masked and unmasked GERD). Newly developed GERD after successful H. pylori therapy is a kind of unmasked GERD arising after cure of infection (de novo unmasked GERD). The possible mechanism of the improvement of cured GERD is normalized hyperacidity associated with an improved cytokine-somatostatin-gastrin system followed by normalized G-cell activity and parietal cell mass. Preexisting GERD is not a reason to avoid eradication therapy. De novo unmasked GERD develops in a substantial proportion of patients with cured infection. The possible mechanism is increased acid exposure in the esophagus due to gastric acid increase, which is caused by a loss of neutralizing effect by ammonia, normalized cytokine-acid suppression and improvement of corpus atrophy. De novo unmasked GERD is important because GERD is recurrent and may induce adenocarcinoma of the esophagus. However, it is expected that cure of infection lowers gastric cancer incidence. Eradication therapy is recommended irrespective of the possibility that de novo unmasked GERD may have a slight increase of the risk of esophageal adenocarcinoma.
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PMID:Active and inactive gastroesophageal reflux diseases related to Helicobacter pylori therapy. 1295 Jun

Omeprazole, a proton pump inhibitor (PPI), is widely used in treatment of peptic ulcer, gastro esophageal reflux disease and eradication of Helicobacter pylori. PPIs inhibit final gastric acid secretion stage by blocking H+/K+-ATPase. But the mechanism except for gastric antisecretory effect has not understood clearly. So, we examined the effects of omeprazole on the levels of gastrointestinal peptides (somatostatin, motilin, gastrin, vasoactive intestinal peptide (VIP), substance P (SP) and calcitonin gene-related peptide (CGRP)) in plasma from healthy subjects. After a single oral administration of omeprazole, the plasma omeprazole concentration was highest at 120 min. Omeprazole caused a significant increase of plasma somatostatin-immunoreactive substance (IS) levels at 60-240 min and plasma motilin-IS levels at 120-180 min, compared with a placebo group, respectively. The physiological release of plasma gastrin-IS was reduced by the administration of omeprazole at 60 min, but the medicine did not alter the levels of VIP-, CGRP- and SP-IS. These results suggested that the pharmacological effects of omeprazole on regulation of gastrointestinal function are closely related to changes of somatostatin-, motilin- and gastrin-IS levels in human plasma.
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PMID:Omeprazole raises somatostatin and motilin in human plasma. 1568 3


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