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)

Chromogranin A (Cg A) is a protein that is coreleased with peptide hormones from gut endocrine cells and tumors. Plasma levels of Cg A, pepsinogen group I, and gastrin were measured in 31 patients with gastrinoma. Mean Cg A level in 10 patients with gastrinoma who were not operated on was 169 +/- 32 ng/mL, while in 9 control patients it was 28 +/- 5 ng/mL. In 18 patients with gastrinoma with residual tumor after total gastrectomy, the mean Cg A level was 45 +/- 6 ng/mL, and in 10 patients with normal gastrin levels after total gastrectomy and tumor excision, the mean Cg A level was 40 +/- 4 ng/mL. In 7 patients in whom pregastrectomy and postgastrectomy Cg A levels were measured, the mean reduction was 94 +/- 27 ng/mL, or 66%. There was no correlation between Cg A levels and amount of tumor, presence of metastases, or multiple endocrine neoplasia type I syndrome. There was a significant correlation between Cg A and pepsinogen I levels but no correlation between Cg A and gastrin levels. The results suggest that the elevated plasma Cg A levels in patients with gastrinoma are determined primarily by the trophic effects of gastrin on gastric enterochromaffinlike cells rather than by corelease from the gastrin-producing tumor itself.
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PMID:Source of plasma chromogranin A elevation in gastrinoma patients. 232 9

In dispersed gastric chief cells from guinea-pig stomach, binding of iodinated cholecystokinin octapeptide (125I-CCK-8) was relatively slow, temperature-dependent, to a single class of binding sites and inhibited by various gastrin- and CCK-related agonists and receptor antagonists. Binding of iodinated gastrin-I (125I-gastrin-I) was moderately rapid, temperature-dependent, to a single class of binding sites, and inhibited by various gastrin and CCK-related agonists and receptor antagonists. Gastrin-I as well as C-terminal fragments of CCK containing from eight amino acids (CCK-8) to four amino acids (CCK-4) stimulated pepsinogen secretion and inhibited binding of 125I-CCK-8 and 125I-gastrin-I. In addition, each of five different receptor antagonists inhibited binding of 125I-CCK-8 and 125I-gastrin-I and inhibited pepsinogen secretion stimulated by CCK-8 or gastrin-I. With each of eight different agonists and with each of five different antagonists the value of IC50 for inhibition of binding of 125I-CCK-8 was not significantly different from the value of IC50 for inhibition of binding of 125I-gastrin-I, indicating that in gastric chief cells the sites to which 125I-CCK-8 binds are the same sites to which 125I-gastrin-I binds. With the agonists as well as with the antagonists, however, there was no consistent relationship between the ability of a particular agent to inhibit binding and its ability to modify pepsinogen secretion, indicating that in gastric chief cells the sites that bind 125I-CCK-8 and 125I-gastrin-I are not the receptors that mediate stimulation of pepsinogen secretion by CCK-8 or by gastrin-I.
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PMID:Binding of 125I-CCK-8 and 125I-gastrin-I to dispersed chief cells from guinea-pig stomach. 232 95

Gastric mucosal histology and function were evaluated in 57 Italian subjects with dermatitis herpetiformis (DH), by means of multiple endoscopic biopsies, gastrin and pepsinogen I (Pg I) serum levels, and parietal cell antibodies (PCA). One hundred and forty-nine patients with nonulcer dyspepsia served as reference population for the prevalence of atrophic gastritis of the body. Seventeen DH patients (30%) and 23 controls (15.4%) showed atrophic gastritis of the body mucosa (p less than 0.05). Nine of the DH patients with atrophic gastritis of the body also had atrophic changes in the antrum. Six patients, all with severe atrophic gastritis, had high gastrin levels and PCA; five of these six also had low Pg I levels. We found an increased prevalence of abnormal indirect function tests among patients with atrophic gastritis is due to the younger age of the patients in our series. Thus, atrophic gastritis can be detected early on a histologic basis, but functional impairment occurs later, as the mucosal damage increases in severity.
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PMID:Gastric histology and function tests in Italian patients with dermatitis herpetiformis. 233 46

Anatomically, functionally, and clinically, peptic ulcer patients are a heterogeneous group of subjects. These patients can be classified according to the anatomic localization of the niche. The functional state of the gastric mucosa was studied in 30 gastric ulcer patients, 25 duodenal ulcer patients, and 10 normal controls. The classification of the first group was based on Johnson's criteria, with the following results: 10 individuals were type I, 10 were type II, and 10 were type III. Pepsinogen I levels and gastric acid secretion were measured in all 65 subjects under basal conditions and after subcutaneous pentagastrin stimulation. Both basal and stimulated serum pepsinogen I values were significantly higher (p less than 0.05) in gastric ulcer type III patients than in the other four groups. These values in gastric ulcer type I were similar to those of the controls. Gastric ulcer type II patients showed an intermediate functional state similar to that of duodenal ulcer patients. In both gastric ulcer type II and duodenal ulcer patients, the basal and stimulated pepsinogen I levels were significantly higher (p less than 0.05) than those found in controls, whereas the basal serum gastrin levels were similar in the five groups. In conclusion, different HCl and pepsinogen I secretory patterns, with functional heterogenicity of the gastric mucosa, are shown here for the anatomically defined gastric ulcer subsets.
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PMID:Different HCl and pepsinogen I secretion patterns in anatomically defined gastric ulcer subsets. 233 56

Post-natal malnutrition was induced in rats using the expanded litter model. Pepsinogen secretion of isolated gastric glands in response to several secretagogues was measured. Malnourished 19-day-old pups showed no response to carbachol, CCK-8, gastrin, secretin and ionophore A23187 compared to well-nourished animals, but showed comparable secretion of pepsinogen after stimulation with dibutyryl cAMP (DiBcAMP). Hydrocortisone treatment for 48 h caused increased pepsinogen accumulation and elevated pepsinogen secretory responsiveness to carbachol and secretin of gastric glands isolated from post-natal malnourished pups. Our results indicate that isolated gastric glands obtained from well-nourished rat possess two functionally distinct receptors for gastrin and C-terminal fragment of CCK. Our study supports the concept that in malnourished rats there is a decreased number of binding sites or/and some post-receptor defects. Pepsinogen release mechanisms remain unaffected.
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PMID:The effect of post-natal malnutrition on pepsinogen secretion receptors in weanling rats. 235 49

We report two cases of duodenal ulcer (DU) identified at endoscopy in a pair of dizygotic twins; their outstanding clinically recognizable features were a very early onset, a great familiar occurrence, a lack of triggering conditions (drugs, burns, stress, sepsis, respiratory distress), normal serum levels of gastrin and pepsinogen I, inadequate response to medical treatment with H2-receptor antagonists, but satisfactory response to associated therapy with H2-receptor antagonists and sucralfate. Results of this study show that examined twins were affected by a form of early-onset primary DU, probably inherited like an autosomal dominant disorder with high degree of penetrance, associated with normal serum pepsinogen I and gastrin; in this form of Du a decreased tissue resistance of duodenal mucosa is likely more important, pathogenically, than an increased peptic secretion. At present long-term prognosis of our patients is unknown.
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PMID:[Duodenal ulcer in 2 dizygotic twins]. 237 69

We present 28 children, 4 to 14 year-old, with duodenal ulcer; there were 21 males and 7 females. In 16 cases, after stimulation with pentagastrin, basal pepsinogen I (PG1), basal gastrinemia and basal acid output (BAO) and maximal acid output (MAO) were measured. Compared to controls, the mean levels of PG1 and gastrin were significantly higher in the patients; 12 children (80%) had high levels of PG1 and the remaining 3 (20%) had normal levels. The blood group O was the most prevalent: 64% of the cases.
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PMID:[Duodenal ulcer in children. Apropos of 28 cases]. 237 56

Although cholecystokinin (CCK) has been reported to stimulate pepsinogen secretion, this action has been poorly characterized. To assess the ability of CCK to regulate mammalian pepsinogen secretion, guinea pig fundic mucosa was incubated in Ussing chambers with CCK-8, carbamylcholine, and pentagastrin, and with cholinergic and CCK antagonists. CCK-8 stimulated pepsinogen secretion at 10(-10) M, with an ED50 of 10(-9) M and maximally (26-fold over basal) at 10(-8) M. Carbachol stimulated pepsinogen and acid secretion with an ED50 of 3 x 10(-7) M and maximally at 10(-6) M. Pentagastrin (10(-9) M-10(-6) M) did not affect acid or pepsinogen secretion, whereas gastrin-I (10(-6) M) stimulated acid secretion slightly but did not alter pepsinogen secretion. L364, 718 (10(-5) M), a specific CCK peripheral receptor antagonist, abolished all pepsigogic effects of 3 x 10(-9) M CCK-8 without altering basal acid or pepsinogen secretion or mucosal electric characteristics. L364,718-treated tissues unresponsive to CCK-8 nevertheless secreted pepsinogen and acid in response to 3 x 10(-7) M carbachol identically to control carbachol-treated preparations. Atropine (10(-5) M) blocked the response to 3 x 10(-7) M carbachol without inhibiting 10(-9) M CCK stimulation. These results support a specific receptor-mediated role for cholecystokinin in the physiologic regulation of guinea pig pepsinogen secretion.
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PMID:Effects of cholecystokinin and cholinergic receptor blockade on guinea pig pepsinogen secretion. 240 88

When dispersed chief cells from guinea pig stomach were first incubated with cholecystokinin (CCK), washed, and then reincubated with CCK in fresh incubation solution, the stimulation of pepsinogen secretion and the rise in intracellular calcium concentration during the second incubation were reduced. CCK did not cause residual enzyme secretion but caused desensitization that was rapid, temperature dependent, dependent on extracellular calcium, reversible with time, and prevented but not reversed by CCK receptor antagonists. Cholecystokinin octapeptide (CCK-8) caused desensitization over the same range of concentrations that stimulate pepsinogen secretion, whereas the concentration of gastrin required to cause maximal desensitization was greater than that required to cause maximal stimulation of enzyme secretion. CCK-8 caused heterologous desensitization of pepsinogen secretion stimulated by agonists that interact with receptors to cause mobilization of cellular calcium and activation of protein kinase C or by agonists that bypass receptors to activate these mediators directly; however, CCK-8 did not induce desensitization of the stimulation caused by any secretagogue whose actions are mediated by adenosine 3',5'-cyclic monophosphate. Because CCK-8 caused greater desensitization of secretion stimulated by agonists that interact with receptors than by agonists that bypass receptors, it is likely that receptor modulation as well as a postreceptor action contribute to the ability of CCK to cause desensitization of pepsinogen secretion from chief cells.
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PMID:Cholecystokinin-induced desensitization of pepsinogen secretion from chief cells. 249 49

32 children (mean age 12 years, range 6-18) with non-specific abdominal pain and Campylobacter pylori positive gastritis received a six week course of daily oral amoxycillin (50 mg/kg) and tinidazole (20 mg/kg). Before treatment and one month after stopping treatment, endoscopic biopsy samples were taken from the antral mucosa and serum C pylori IgG antibody, pepsinogen I, and gastrin levels were measured in fasting blood samples. One month after treatment 30 children (94%) were cleared of C pylori and gastritis had resolved in 27 (84%) and was improved in the remaining 5. Serum IgG, pepsinogen I, and gastrin levels were significantly decreased after treatment. Of 12 children assessed at six months, 9 remained free of C pylori. Increases or decreases in IgG level indicated clearance or recurrence, respectively, of C pylori.
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PMID:Amoxycillin plus tinidazole for Campylobacter pylori gastritis in children: assessment by serum IgG antibody, pepsinogen I, and gastrin levels. 256 7


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