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)

Exposure of the stomach to tumoricidal doses of radiation is associated with functional and morphological changes. The experimental data have been mainly obtained from studies of whole body irradiation of the stomach. We investigated the separate effect of irradiation on the surgically exposed stomach with doses of between 3 and 30 Gy. A dose-dependent decrease in free and total acidity was observed with relatively low doses (5-9 Gy). Serum pepsinogen and serum gastrin levels increased following irradiation with doses ranging from 5 to 15 Gy. Two phases of increased regenerative activity were documented (between the 1st and 3rd weeks and between the 4th and 8th weeks). No radioprotective effect was observed when sucralfate or misoprostol were utilized. Further investigations are mandatory in order to find an effective radioprotector for the irradiated stomach.
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PMID:Functional and morphological alterations following isolated rat stomach irradiation. A model for estimation of radiation injury. 297 4

CCK-octapeptide (CCK-8) (EC50 = 0.5 nM), in the presence of Li+, increased 3H-inositol phosphate (IP) accumulation in guinea pig gastric glands prelabeled with 3H-inositol. CCK-8 desulfate, human gastrin I and pentagastrin were much less potent than CCK-8. Antagonists of CCK receptors such as proglumide, dibutyryl-c-GMP and CBZ-Tyr (SO3H)-Met-Gly-Trp-Met-AspNH2 shifted the CCK dose response curve to the right. However, histamine (H1 and H2), cholinergic, substance P and alpha- and beta-adrenergic receptor antagonists had no effect on 3H-IP accumulation induced by CCK. The results suggest that CCK receptor activation in gastric glands leads to an enhanced breakdown of inositol phospholipids which may relate to calcium mobilization and pepsinogen secretion.
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PMID:Cholecystokinin receptor mediated hydrolysis of inositol phospholipids in guinea pig gastric glands. 298 60

The effect of omeprazole on gastric acid and pepsin secretion and fasting serum gastrin and serum pepsinogen I levels was studied in 12 healthy volunteers. Omeprazole, 40 mg enteric-coated granules, or placebo was given once daily for nine days in a double-blind crossover study design. Twenty-four hours after a single dose of omeprazole, mean basal and mean pentagastrin-stimulated acid output decreased significantly. This effect was more pronounced after nine days of treatment. Basal pepsin output was significantly reduced only in those subjects with basal anacidity during omeprazole treatment. Stimulated pepsin output was slightly reduced after a single dose but unaltered after nine days of omeprazole. Fasting serum gastrin and serum pepsinogen I levels increased significantly during omeprazole treatment. It is concluded that omeprazole is a potent and selective inhibitor of gastric acid secretion, probably without a direct effect on pepsin secretion. However, in cases of basal anacidity during omeprazole administration, basal pepsin secretion is reduced. During omeprazole treatment, fasting serum levels of gastrin and pepsinogen I rise.
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PMID:Effect of single and repeated doses of oral omeprazole on gastric acid and pepsin secretion and fasting serum gastrin and serum pepsinogen I levels. 308 61

The effects of inhibiting polyamine synthesis on the functional development of the gastric mucosa were studied in rats from 5 to 40 days old. They were treated from day 14 after birth with alpha-difluoromethylornithine (DFMO) at a concentration of 2% in the drinking water of mothers and pups. The rats were weaned on day 18. Basal acid and pepsin secretion, oxyntic gland mucosal pepsinogen content, and antral gastrin content followed similar developmental patterns in control animals. Levels of these parameters remained measurable but low until around the time of weaning, when dramatic log linear rises were observed. DFMO failed to delay the onset of the rises in any of these maturational indices. Ornithine decarboxylase (ODC) activity in the oxyntic gland mucosa was low but discernible in rats of every age studied. DFMO significantly reduced ODC activity at every age except 40 days, where there was no difference from control values. Our results suggest that ODC activity in the rat gastric mucosa does not change appreciably during neonatal development and that inhibiting putrescine synthesis from its precursor ornithine by DFMO treatment does not prevent or delay gastric mucosal maturation.
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PMID:Role of ornithine decarboxylase in functional development of rat gastric mucosa. 310 30

The effect of trimoprostil, an analogue of prostaglandin E2, on gastric secretion was studied in healthy volunteers in comparison with that of cimetidine. Graded doses of 50, 250, 500 and 750 micrograms were given p.o. for trimoprostil and 200 mg for cimetidine. Basal secretion was significantly depressed at doses larger than 500 micrograms of trimoprostil but not by 200 mg of cimetidine probably due to the method of gastric analysis adopted in the study. In amyl-oxy-carbonyl (AOC)-tetragastrin stimulated gastric secretion, 500 micrograms of trimoprostil depressed acid output significantly, but did not affect pepsin output which was depressed, however, at 750 micrograms. On the other hand cimetidine markedly inhibited AOC-tetragastrin stimulated acid and pepsin secretion. Some difference was also recognized between trimoprostil and cimetidine concerning the mechanism of inhibitory action. Serum concentration of trimoprostil measured at 60 min after oral administration varied dose-dependently and antisecretory effects were also found to be dose-related. Serum gastrin and pepsinogen I were not affected either by trimoprostil or cimetidine. These results indicate that trimoprostil showed inhibitory effect on gastric secretion at doses larger than 500 micrograms for acid, and at doses larger than 750 micrograms for pepsin.
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PMID:Effect of trimoprostil on gastric secretion in man. 314 Aug 24

A new experimental model, the isolated perfused antrectomized pig stomach with intact vagal innervation, was shown to produce pepsinogen and gastric acid upon electrical stimulation of the vagus nerves and by intravascular administration of carbachol (from a basal value of 111 +/- 24 units of pepsin per minute and 0.044 +/- 0.012 mEq H+/min to 393 +/- 75 units of pepsin per minute and 0.102 +/- 0.022 mEq H+/min upon vagal stimulation). Vagal stimulation also increased the release of the neuropeptide gastrin-releasing peptide to the venous effluent from 0.42 +/- 0.12 to 3.1 +/- 0.95 pmol/min. Intravascular infusions of gastrin-releasing peptide at a concentration of 10(-8) mol/L resulted in a threefold increase in pepsinogen secretion and a small increase in acid output. Because gastrin-mediated effects of gastrin-releasing peptide are excluded with this preparation, our results show that gastrin-releasing peptide acts either directly or through another unknown local mediator on the pepsinogen-secreting cells. Gastrin-releasing peptide may thus participate in the vagal control of pepsinogen secretion.
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PMID:Role of gastrin-releasing peptide in the neural control of pepsinogen secretion from the pig stomach. 316 90

Pepsinogen (PG) I and PG II levels were determined in sera from 147 patients with pernicious anemia. Race, sex, age, gastrin level, and antibody status did not influence pepsinogen levels. PG I values less than 30 micrograms/L were found in 92% of cases and PG I to PG II ratios less than 3.0 in 82% of cases. At least one of these two results was abnormal in 97% of all patients with pernicious anemia. In comparison, results of other blood tests used in the investigation of pernicious anemia were less often abnormal. Serum gastrin level exceeded 200 ng/L in 90% of patients with pernicious anemia and was second to pepsinogen abnormality in diagnostic sensitivity. Results for anti-intrinsic factor antibody were positive in 73% of cases and anti-parietal cell antibody in only 52%. Although its specificity is limited, the presence of low PG I level and/or low PG I-PG II ratio is currently the most sensitive serum indicator for pernicious anemia, and absence of both can be taken as a strong argument against the diagnosis. This highly sensitive test can be combined further with the highly specific serum anti-intrinsic factor antibody test for the presumptive diagnosis of pernicious anemia when definitive tests (the Schilling test or gastric analysis for intrinsic factor) cannot be done or results are inconclusive.
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PMID:Pepsinogens and other serum markers in pernicious anemia. 317 65

Serum pepsinogen 1, serum gastrin, ABO blood groups, secretor status of ABH blood group substances and behavioral factors were studied in 15 patients with duodenal ulcer and 61 their relatives affected and unaffected to duodenal ulcer. Duodenal ulcer patients had hyperpepsinogenemia 1 either with or without a positive family history of duodenal ulcer. Serum gastrin level was higher in duodenal ulcer patients and unaffected relatives with a positive family history of duodenal ulcer than those with a negative family history. Non secretor status was frequently observed in duodenal ulcer patients with a positive family history. There was no difference in behavioral factors between duodenal ulcer patients and unaffected relatives with a positive family history. It is concluded that genetically determined variables such as hyperpepsinogenemia 1 and non secretor status play an important role on the susceptibility to duodenal ulcer in subjects with a positive family history, and hypergastrinemia may be subclinical marker of familial aggregation of duodenal ulcer.
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PMID:Serum pepsinogen 1, gastrin, ABO blood groups, secretor status of ABH substances and behavioral factors in patients with duodenal ulcer and their relatives. 319 59

Blood gastrin and pepsinogen responses to a single infection with 100,000 Ostertagia ostertagi infective larvae in lactating dairy cows were investigated. None of the infected cows showed signs of clinical ostertagiasis, nor was there any difference in live weight gain, milk yield or faecal egg count between groups. Pepsinogen levels of the infected group were significantly elevated between days 3 and 24 after infection (peak 1041 mU tyrosine; day 14). In contrast, there was no significant difference in blood gastrin levels between infected and control animals suggesting that few adult worms had become established in the former group. These data are compared with the increases in both gastrin and pepsinogen levels recorded in susceptible calves exposed to the same level, pattern and strain of ostertagia infection in a previous experiment. It is suggested that gastrin assay may be of value in adult cattle for indicating when elevated pepsinogen levels are merely associated with a rise in larval intake and not with the establishment of large adult worm burdens.
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PMID:Blood gastrin and pepsinogen responses to subclinical infection with Ostertagia ostertagi in adult dairy cattle. 322 46

Pathophysiological changes in the ruminant abomasum caused by Ostertagia infections include changes in the activity and concentration of gastrointestinal enzymes and hormones. Under certain circumstances, increases in concentration also occur in the bloodstream and, as such, are detectable. Determination of serum pepsinogen levels is useful in evaluating the risk or presence of ostertagiasis Type I in a herd. It seems less reliable when used to diagnose (pre) ostertagiasis in individual animals. Measurement of the concentration of other zymogens is not useful. The variations in methodology to determine pepsinogen levels (e.g. biochemical and immunological measurements) are discussed. Serum gastrin levels are, generally, increased in animals with ostertagiasis. At present, gastrin is mainly determined by RIA assays using human gastrin antibodies, but few baseline data are available on normal levels in ruminants. The use of gastrin determination as a diagnostic tool in Ostertagia-infected ruminants is limited.
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PMID:Evaluation of abomasal enzyme and hormone levels in the diagnosis of ostertagiasis. 328 63


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