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)

To assess the effect of malnutrition on gastric acidity and gastric bacterial colonization, we studied 35 severely malnourished Bangladeshi children before (0 wk) and after (3 wk) they received nutritional rehabilitation for 3 wk. These results were compared with those obtained from a similarly examined group of 20 better-nourished Bangladeshi children. Gastric acid output, both basal and after betazole stimulation, was significantly lower in the malnourished group at 0 wk compared with the better-nourished children (p less than 0.01): basal 0.22 vs. 0.52 mEq HCl/h and stimulated 0.90 vs. 2.5 mEq HCl/h. Both the concentration of acid and the rate at which gastric juice was secreted were decreased in the malnourished group but serum gastrin levels were not significantly different. After 3 wk, the malnourished children had improved from 61% (+/- 9.0%; SD) to 81% (+/- 8.1%) of expected weight-for-height and were not significantly different than the better-nourished group (86% +/- 11%). Nevertheless, gastric acid concentration remained depressed in the 3-wk group, although the rate of gastric juice secretion equaled levels observed in the better-nourished group. None of the better-nourished children had detectable gram-negative bacterial colonization of their gastric juice. In contrast, 26 of 32 (81%) malnourished children at 0 wk were colonized--even after betazole stimulation, 11 of 33 (33%) gastric juice samples yielded viable organisms--suggesting that the decrease in gastric acid output greatly reduced the gastric acid barrier. Interestingly, only 9 of 20 (45%) better-nourished children had gastric juice with basal pH values below 4.0, suggesting that the gastric acid barrier may be an intermittent defense factor in Bangladeshi children.
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PMID:Decreased gastric acid secretion and bacterial colonization of the stomach in severely malnourished Bangladeshi children. 312 29

The cause of the physiologic hypochlorhydria and hypergastrinemia of the newborn is not understood. The effect of antral acidification on basal serum gastrin was studied in 32 anesthetized Landrace piglets divided into four groups of eight animals each: Group A, 1 to 7 days old; Group B, 8 to 15 days old; Group C, 16 to 24 days old; and Group D, 25 to 48 days old. After a 2-hr fast, halothane anesthesia was administered. Inflow and outflow cannulae were inserted into the gastric lumen to create an intact isolated gastric antrum. HCl in saline (pH 2.5) was infused (10 cc/min) for 15 min and drained by continuous suction. The effluent was confirmed to be pH 2.5. Portal venous blood samples were obtained at basal levels and at 5, 10, and 15 min and assayed for gastrin. All groups had markedly elevated serum gastrin levels, as compared to normal adult values, in the basal state. Basal gastrin levels declined with increasing age to approach adult values by 7 weeks. Following antral acidification in Groups A, B, and C, there was a significant reduction in serum gastrin. All suppressed values remained significantly higher than adult basal, however. There was no significant change in gastrin levels in Group D with acidification.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of antral acidification on serum gastrin levels in neonatal pigs. 341 51

Two patients with chronic abdominal pain and fasting hypergastrinemia had increases in serum gastrin of 440 and 300 pg/ml after injection of 2 U/kg Secretin-KABI. Both subsequently proved to have pentagastrin-fast achlorhydria. Intragastric instillation of 0.1 N HCl suppressed serum gastrin concentration by greater than 60%. In both, the pancreas was normal by sonography or computed tomography (CT) scan and at laparotomy in one. Both are currently asymptomatic 12 and 18 months later. We conclude that achlorhydria may be associated after injection of Secretin-KABI with a false-positive rise in fasting serum gastrin concentration of greater than 200 pg/ml and that gastric analysis for hypochlorhydria should be performed before secretin provocation testing.
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PMID:False-positive secretin-KABI provocation test associated with achlorhydria. 341 78

In chloralose anesthetized dogs and decerebrated dogs whose pyloric sphincter was submucosally ligated, the pancreatic exocrine secretory response to antral distension was studied. Distensions of the antral pouch with Tyrode's solution and 0.1 N HCl caused graded rises in pancreatic flow and protein and bicarbonate outputs. The serum gastrin concentration gradually rose after the distention with Tyrode's solution, while no rise in serum gastrin was elicited by acid distension. After cervical vagotomy, a reduced pancreatic response persisted but no rise in the serum gastrin was seen. After splanchnicectomy following vagotomy, the pancreatic response became greater than before splanchnicectomy. This pancreatic response was observed even after caeliac and superior mesenteric ganglionectomies, but was completely abolished by an external tight ligature around the pyloric sphincter, or by administration of hexamethonium or atropine sulfate. The results suggest the existence of an antropancreatic short reflex in addition to a long route vago-vagal reflex.
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PMID:Effects of antral distension on pancreatic exocrine secretion in dogs: evidence for a short reflex. 343 Aug 72

A series of 30 gastric endocrine tumours has been revised in the light of available available cytologic and clinicopathologic information. Among 24 well differentiated endocrine tumours-16 with and 8 without chronic atrophic gastritis (CAG)-3 gastrin cell tumours have been distinguished from 21 argyrophil carcinoids, 15 of which showed light- and/or electronmicroscopy patterns of enterochromaffin-like (ECL) cell tumours, 2 of EC cell tumours and 1 of D1/P cell tumour. One case of mixed carcinoid/adenocarcinoma and 5 cases of endocrine carcinomas, 4 poorly and 1 moderately differentiated, were also identified. Achlorhydria, due to type A CAG or HCl-suppressing drugs, and bombesin hyperstimulation are among possible factors inducing G cell hyperfunction and/or hyperplasia. Hypergastrinaemia is among causative agents of argyrophil ECL cell hyperplasias and, possibly, of tumours of the oxynticopeptic mucosa, while chronic inflammation and gland atrophy with or without concomitant hypergastrinaemia are important factors in inducing both hyperplastic and tumour argyrophil growths in CAG mucosa.
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PMID:Gastric carcinoids and related endocrine growths. 353 79

The aim of this study was to determine whether mucosal antrectomy, which preserves antropyloric motility, would enhance the antiulcer properties of proximal gastric vagotomy (PGV). Hydrochloric acid and gastrin secretion were studied in five dogs before and after PGV and mucosal antrectomy, while the response to the Mann-Williamson operation (an ulcer-producing operation) was evaluated in four control dogs with intact stomachs, five dogs with PGV alone, and six dogs with PGV plus mucosal antrectomy. Proximal gastric vagotomy and mucosal antrectomy decreased mean +/- SEM basal and pentagastrin-stimulated acid secretion from 4.3 +/- 1.3 to 0.4 +/- 0.3 mEq/hr and from 21 +/- 0.7 to 7.4 +/- 1.8 mEq/hr, respectively (p less than 0.05). Basal plasma gastrin was altered little by the operation (68 +/- 9.7 pg/ml before, 58 +/- 11 pg/ml after; p greater than 0.05) but the 4-hour integrated plasma gastrin response to a 200 gm meat meal decreased from 13 +/- 1.8 to 3.3 +/- 0.7 ng X min/ml (p less than 0.05). Only one of six dogs with mucosal antrectomy and PGV developed peptic ulcer after the Mann-Williamson operation, whereas four of five with PGV alone and three of four controls developed ulcers (p less than 0.05, PGV alone versus PGV and mucosal antrectomy). In conclusion, PGV and mucosal antrectomy decreased acid secretion and postcibal gastrin response and provided greater protection against peptic ulcer than PGV alone.
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PMID:Proximal gastric vagotomy and mucosal antrectomy: effect on gastric acid secretion, plasma gastrin, and experimental ulcerogenesis in the dog. 357 53

The presence of immunoreactive (ir)-bombesin in bovine adrenal medulla, isolated adrenal chromaffin cells and subcellular fractions of the adrenal medulla was demonstrated using a specific antibody to the synthetic peptide. High levels of ir-bombesin were detected in acid (HCl) extracts of the adrenal tissue (27 pmol/g) and isolated cells (0.35 pmol per 10(6) cells). Subpopulations of adrenal chromaffin cells were also obtained by centrifugation of the original cell preparation through a stepwise bovine serum albumin gradient (cell layers I, II and III). The highest concentration of ir-bombesin (0.77 pmol/10(6) cells) was found in a cell population (cell layer I) enriched in noradrenaline (adrenaline/noradrenaline ratio of 0.6). At the subcellular level, ir-bombesin was mainly concentrated in the secretory granules (0.61 pmol/mg protein) along with catecholamines (1097 nmol/mg protein), but a relatively high concentration of ir-bombesin (0.26 pmol/mg protein) was also found in the microsomal fraction. Isolation and high performance liquid chromatography (HPLC) analysis of adrenomedullary ir-bombesin revealed the presence of four molecular forms, one of them corresponding to gastrin releasing peptide (GRP), another one (major peak) eluting closely to synthetic neuromedin B and another one coeluting with GRP-(18-27). HPLC analysis of the molecular forms of ir-bombesin in the microsomes and secretory granules indicated that GRP- and neuromedin B-like materials can be generated between the two fractions.
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PMID:Bombesin-like immunoreactivity in bovine adrenal medulla. 395 50

Acid secretory behavior as well as gastrin levels were evaluated in 38 cases of chronic duodenitis. Basal HCl secretion was normal in 39% of cases, hypochlorhydria was observed in 29%, and hyperchlorhydria in 32%. Maximal acid output was normal in 71% of patients with duodenitis, decreased in 19%, and increased in 10%. Fasting serum gastrin was always within normal limits. The secretory behavior correlated with age but not with the histological pattern of duodenal mucosa. In chronic duodenitis, normal secretion or hypochlorhydria is the prevailing finding. This does not exclude the possibility of a peptic pathogenetic mechanism which could be involved in the rare cases of chronic duodenitis with hyperchlorhydria. Acid-peptic disease is not etiopathogenetic in the causation of most cases of chronic duodenitis.
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PMID:Is duodenitis always a peptic disease? 400 72

Alkaline secretion from the fundic and antral pouches of the stomach and the loops of proximal and distal duodenum was measured in conscious dogs under basal conditions and after intragastric instillation of HCl solution, meat feeding, or intravenous infusion of various gut hormones. In control tests on fasted dogs HCO-3 output from the duodenal mucosa was severalfold higher than that from the gastric mucosa. Instillation of 10 mM HCl into the stomach resulted in a significant increment in HCO-3 secretion from the gastric pouches and proximal duodenal loops, and this was accompanied by a marked increase in plasma secretin, cholecystokinin (CCK), and pancreatic polypeptide (PP) levels. Meat feeding stimulated HCO-3 secretion from proximal duodenum, and it was accompanied by a significant elevation in plasma gastrin, secretin, CCK, gastric inhibitory peptide, and PP. Among exogenous hormones, the most effective stimulant of HCO-3 secretion was PP, which caused a significant increase in HCO-3 output from the gastric and duodenal mucosa at doses (125-500 pmol X kg-1 X h-1) that raised plasma PP to postprandial levels. CCK in physiological doses (21-85 pmol.kg-.h-1) also stimulated HCO-3 secretion from gastric pouches and proximal duodenal loops. Neurotensin stimulated HCO-3 secretion from both gastric pouches and duodenal loops. In contrast, gastrin or secretin did not affect significantly HCO-3 secretion from the gastroduodenal mucosa. This study provides evidence that some gut hormones, particularly PP, CCK, and neurotensin, may be involved in the physiological stimulation of gastroduodenal alkaline secretion.
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PMID:Gut hormones in stimulation of gastroduodenal alkaline secretion in conscious dogs. 400 49

The effect of histamine on gastrin release was studied in 7 conscious mongrel dogs with chronic gastric and duodenal fistulas. Histamine-2 HCl was infused in doses of 0 (control), 20, 40, 80, and 160 micrograms/kg per h for 2 h on separate days. During the second hour, bombesin 500 ng/kg per h was infused intravenously. Intragastric pH was constantly kept at 2.5 by intragastric titration during each test. Leakage of gastric contents into the duodenum was prevented by a prepyloric balloon passed retrograde through a duodenal fistula. Gastrin release, as expressed by the integrated response during the last 50 min of the bombesin infusion was significantly (P less than 0.05) decreased by all doses of histamine, compared to control. The infusion doses of histamine studied, 20, 40, 80, and 160 micrograms/kg per h reduced bombesin-stimulated gastrin release 16%, 19%, 19%, and 30%, respectively. This effect was blocked by a histamine H-2 but not an H-1 receptor antagonist. We conclude that by an H-2 mechanism, exogenous histamine reduces bombesin-stimulated gastrin release in dog.
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PMID:Intravenous histamine reduces bombesin-stimulated gastrin release in dogs. 405 85


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