Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present study, pancreatic polypeptide (PP) levels both in basal state and after stimulation by meal were determined in 21 controls, 28 patients with gastric ulcer and 21 patients with duodenal ulcer and their correlation with gastric emptying was examined. In patients with gastric and duodenal ulcers, basal levels as well as stimulated of plasma PP during 95 min of observation period were higher than those in controls except for the values at 5 min. As no correlation was seen between integrated PP response (IPPR) to the meal and T1/2 for gastric emptying in any of three groups, it was indicated that gastric emptying has only a minor role in postprandial PP response.
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PMID:Correlation between gastric emptying time and the response of pancreatic polypeptide to test meals in peptic ulcer diseases. 359 Jan 74

The plasma pancreatic polypeptide response to a meal was compared in 6 healthy controls and 30 patients with gastric cancer who had undergone either subtotal gastrectomy or total gastrectomy with radical lymph node dissection including sympathectomy. Twelve patients were reconstructed with Billroth I, 9 patients with Billroth II, 6 patients with a double tract, and 3 patients with Roux-en-Y. Ten patients with a gastric ulcer who had undergone Billroth I gastrectomy including pyloric ring preservation also were examined. Impaired pancreatic polypeptide secretion was noted only in Billroth II and Roux-en-Y patients, where the duodenum is not affected by the passage of meals. Billroth I and double tract patients, in contrast, and an enhanced pancreatic polypeptide secretion. However, in BI patients with pyloric ring preservation the PP response to a meal was almost normal. These findings suggest an important role of the duodenum in the entero-PP axis in man.
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PMID:Possible role of the duodenum in the entero-PP axis. 662 51

The pancreatic polypeptide (PP) response to a protein-rich meal has been studied in similarly aged patients with gastric ulcer, duodenal ulcer, and controls. The response of the gastric ulcer patients was significantly lower at all points than that of the duodenal ulcer patients or controls, which were similar to one another. Vagal stimulation is probably the single most important factor in PP release, and it is possible that diminished PP release in the gastric ulcer patients is a reflection of vagal underactivity.
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PMID:Pancreatic polypeptide release in gastric ulcer. 723 56

We describe a case of gastroparesis after laparoscopic highly selective anterior and posterior truncal vagotomy in a 30-yr-old male with gastric ulcer disease. Motility studies confirmed the diagnosis, and a pancreatic polypeptide sham feeding study suggested that a complete vagotomy may have been inadvertently performed. The experience with this procedure in gastric ulcer disease is extremely limited; review of the literature of laparoscopic highly selective vagotomy describes only two cases with delayed gastric emptying as defined by radiological examination. In view of the paucity of reports, caution is warranted, and this procedure should be undertaken only in the setting of a controlled trial.
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PMID:Delayed gastric emptying after laparoscopic anterior highly selective and posterior truncal vagotomy. 773 92

The present study was carried out to investigate the central effects of pancreatic polypeptide on gastric secretion and gastric ulcer formation in conscious rats. Intracisternal injection of rat pancreatic polypeptide (62.5, 250, and 1000 ng/rat) into pylorus-ligated rats resulted in a dose-dependent stimulation of gastric acid and pepsin secretion. In contrast, intraperitoneal injection of even higher doses of pancreatic polypeptide (250, 1000, and 2500 ng/rat) failed to increase gastric secretion. This stimulatory effect of centrally administered pancreatic polypeptide was completely blocked by vagotomy and by pretreatment with atropine. Intracisternal injection of PP (500-2000 ng/rat) dose-dependently increased the severity of gastric lesions induced by 2-deoxy-D-glucose or indomethacin. In contrast, intraperitoneal injection of PP failed to increase the severity of the gastric lesions induced by 2-deoxy-D-glucose or indomethacin. These results indicate that pancreatic polypeptide is capable of acting centrally in the brain to stimulate gastric acid and pepsin secretion through a vagal, muscarinic pathway and in so doing exerts an ulcerogenic action on the gastric mucosa.
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PMID:Stimulation of gastric secretion and enhanced gastric mucosal damage following central administration of pancreatic polypeptide (PP) in rats. 795 9

The present study included 104 patients with gastric disorders associated with Helicobacter pylori infection. Thirty of them presented with chronic atrophic gastritis (CAG), 30 with gastric ulcer (GU), 20 with adenomatous gastric polyps (AGP), and 24 with gastric cancer (GC). The control group was comprised of 12 practically healthy subjects. We elucidated the role of vascular endothelial growth factor (VEGF) and endocrine cells of gastric mucosa producing glucagon (GC) and pancreatic polypeptide (PPP) in the patients with GAG, GU, AGP and GC prior to and after the surgical intervention and following eradication therapy. It was shown that GAG, AGP, and GC were associated with the persistence of Helicobacter pylori infection and accompanied by hyperplasia of GC and PPP-secreting endocrine cells of gastric mucosa. GU was characterized by hypolasia of VEGF-secreting epithelial cells of the stomach and GC and PPP-secreting endocrine cells of gastric mucosa. The levels of VEGF, GC and PPP that directly or indirectly realize their pathological properties through H. pylori, Bcl-2, and proapoptotic protein BAX proved to be of high prognostic value as regards the evolvement and clinical course of gastric disorders associated with Helicobacter pylori infection. The study demonstrated that adequate eradication therapy in patients with H. pylori-associated diseases of the stomach significantly reduces the number of gastric cells secreting VEGF and has practically no effect on the amount of GC and PPP-producing endocrine cells of gastric mucosa.
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PMID:[The role of epitheliocytes secreting vascular endothelial growth factor, pancreatic polypeptide and glucagon in the development of oncological diseases of the stomach]. 2264 62