Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastric acid secretion was studied in 13 Basenji dogs with immunoproliferative enteropathy. Considerable variation in the severity of gastritis and enteritis existed among dogs. Basenji dogs were categorized into two groups on the basis of postmortem gastric and intestinal histology (group I, gastritis and enteritis; group II, only enteritis). Pentagastrin-induced gastric acid secretory capacity was increased (P less than 0.002) in group II dogs as compared to healthy Beagle controls. Gastric acid secretory capacity of Basenji dogs with gastritis and enteritis (group I) was not different from that observed in control dogs. Basal serum gastrin concentrations and secretin-stimulated serum gastrin concentrations of either group of Basenji dogs did not differ from controls. On the basis of symptomatology, Basenji dogs with diarrhea had significantly increased basal and postsecretin stimulation gastrin concentrations (P = 0.01) when compared with asymptomatic Basenji or healthy control dogs. These findings support a potential role for altered gastric acid secretory capacity in the pathogenesis of immunoproliferative enteropathy of Basenji dogs. Results of the secretin stimulation studies support previous pathologic studies that failed to detect gastrin-secreting tumors. Incorporated into this investigation was a trial to determine whether the combination of oxymorphone and acepromazine could be used for acid secretory studies. Compared to pentobarbital, which has been frequently used for acid secretory studies in a research setting, the drug combination resulted in increased gastric fluid volumes, a comparative increase in acid secretion, and a rapid uneventful recovery. We conclude that the combination of oxymorphone and acepromazine provides an acceptable means of restraint in dogs undergoing acid secretory studies.
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PMID:Gastric acid secretion in Basenji dogs with immunoproliferative enteropathy. 202 13

Achlorhydric atrophic gastritis occurs in approximately 25% of patients with dermatitis herpetiformis (DH). The effect of gluten withdrawal on the gastric condition was studied in 35 patients, with a control group of 20 patients continuing their habitual diet. Gastrointestinal examinations were performed initially and repeated after about 1 3/4 years. Adherence to the diet was confirmed by dietary interviews, improvement of malabsorption test results and intestinal villous structure, and decreased dapsone requirement. Neither the non-restricted diet nor the gluten-free diet had any effect on gastric morphology, the ability to secrete gastric acid, serum gastrin levels, or the frequency or titres of circulating parietal cell antibodies. The findings indicate that gluten is not responsible for the perpetuation of the gastric affection in DH, in contrast to the enteropathy.
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PMID:Influence of gluten-free diet on the gastric condition in dermatitis herpetiformis. 399 62

Motilin, pancreatic polypeptide and gastrin blood concentrations in response to drinking water have been studied in 40 patients with functional bowel disease and compared with results in two groups of healthy control subjects. Patients with slow transit constipation and idiopathic megacolon showed impaired motilin release. Pancreatic polypeptide release was reduced in patients with slow transit constipation, but increased in those with functional diarrhoea. Gastrin release was impaired in all groups complaining of chronic constipation. Circulating motilin, pancreatic polypeptide and gastrin concentrations appear to bear some relationship to intestinal transit time in patients with functional bowel disorders.
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PMID:Positive correlation between symptoms and circulating motilin, pancreatic polypeptide and gastrin concentrations in functional bowel disorders. 405 4

The individual daily intake of gluten was calculated in 45 patients with dermatitis herpetiformis (DH) on the basis of a depth interview about food habits. Gastric and small intestinal morphology and function were studied concurrently. Mean daily gluten intake was estimated to be 15 g, a figure which corresponds well to the average gluten intake in Sweden. There was a significant correlation between the degree of morphological mucosal changes of the small intestine and the quantity of gluten ingested. All patients with jejunal villous atrophy consumed more than 10 g gluten daily and all but one patient with normal jejunal villous structure had a gluten intake of less than 10 g/d. The findings suggest a dose-dependent effect of gluten on the intestinal mucosa. Conversely, the daily gluten intake was not correlated to gastric morphology, gastric acid secretion, serum gastrin levels or serum parietal cell antibodies. Patients with reduced ability to secrete gastric acid did not differ from the remaining patients in this respect. Whereas the coeliac-like enteropathy in DH seems to be caused by ingested gluten, the frequently occurring achlorhydric atrophic gastritis must be assumed to be of different immunopathogenesis.
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PMID:Influence of the amount of dietary gluten on gastrointestinal morphology and function in dermatitis herpetiformis. 646 5

Gastrin influences polyamine synthesis in the enterocytes, which can lead to increased DAO activity. In diabetics with autonomic neuropathy (AN), a higher than normal gastrin concentration was found. However, in diabetics with enteropathy, a low level of plasma DAO activity was discovered. The purpose of this study was to investigate gastrin secretion and to evaluate DAO activity after i.v. injection of heparin in a group of diabetics with AN. Group I consisted of 12 diabetics with AN, group II 20 patients with diabetes without any complications and group III (the control group) 20 patients without diabetes. It was discovered that basal gastrin concentrations were significantly greater in group I (147 pg/ml +/- 76.5) that in groups II (78 pg/ml +/- 55.5)(p < 0.01) and III (61.5 pg/ml +/- 42.6)(p < 0.01). DAO activity was at its lowest in group I (247.1 pmol/min/ml +/- 104.8) and it was significantly different from group II (441 pmol/min/ml +/- 225.9)(p < 0.001) and III (540.7 pmol/min/ml +/- 171.1)(p < 0.001). There were no differences in the mean values of gastrin and DAO activity between group II and III. In group I low DAO activity was accompanied by a proportionally high concentration of the basal gastrin value (r = 0.567). In conclusion, in diabetics with AN, low postheparin plasma DAO activity was accompanied by a high basal gastrin value.
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PMID:[Gastrinemia and heparin stimulated secretion of diamine oxidase on the course of diabetic autonomic neuropathy]. 929 89