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)

Chloralose anaesthetized cats were prepared with fundic and antral pouches. After stimulation with meat extract suspension in the antral pouches, the antral mucosae were collected, homogenized and subjected to subcellular fractionation to produce whole homogenates, debris, mitochondrial, granule and microsomal fractions and the cell supernatant. Total gastrin concentration and the quantities of gastrin components were measured in these cell fractions and compared with values obtained from a group of control animals which were not stimulated. Stimulation significantly increased the concentration of total gastrin in whole homogenates and in the cell supernatant. In whole homogenates the concentrations of gastrin components I, II, III and void volume gastrin all increased significantly after stimulation. In granules the concentration of Component III significantly increased. In microsomes the concentration of Componenet IV increased significantly. In cell supernatant the total amounts of Components III and IV increased significantly. It is concluded there was synthesis of gastrin under the experimental conditions used. The concentrations of those gastrin components which are larger than the predominant storage form (Component III) are increased and these larger components may be biosynthetic precursors. The significant increase in Component IV concentration in the cell supernatant and microsomes may suggest that Component IV is formed at least in part by antral tissue as well as by the known conversion process which occurs in cat blood.
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PMID:The effect of stimulation by meat on gastrins in pyloric antral mucosa of anaesthetized cats. 52 24

Two groups of volunteers (199 in total, 149 of whom were a random sample of an urban population) were examined twice, with a 6-year interval, for the occurrence of parietal cell antibody (PCA) and thyroid microsomal antibodies (TMA). The antibody findings were compared with the antral and fundal gastric mucosal state, and with the fasting serum gastrin-17 level. During the study period, two new PCA and four new TMA cases appeared. There were no significant changes in the state of gastric antral/fundal mucosa in relation to PCA and/or TMA persistence or appearance, as compared with the gastric mucosa changes in the whole random population sample. However, a good correlation was observed between PCA and basal serum gastrin elevation.
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PMID:Relation of parietal cell and thyroid antibodies to the state of gastric mucosa and basal serum gastrin levels during a 6-year follow up. 277 58

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

A decrease in MAO by gastrin stimulation was observed in 13 of 20 hyperthyroid patients. Five of these 13 cases had achlorhydria. The decrease in gastric acid secretion had no relation to the duration of symptoms, serum T3 and T4 levels, serum antithyroglobulin antibody levels and serum antithyroid microsomal antibody levels. Gastroscopy with biopsy was performed in 17 cases. In patients with achlorhydria, macroscopic and histological atrophy was not observed in the body, and parietal cells were present and their succinic dehydrogenase activity was normal. Electron microscopy of the parietal cells of patients with achlorhydria showed that their cells were similar to those in the resting state of healthy subjects with the ability to secrete normal amounts of gastric acid. These findings demonstrate that the decrease in gastric acid secretion in hyperthyroidism is not caused by any structural changes in the gastric mucosa but by functional suppression. In the present experiment, this suppression was found resistant to gastrin. A rise in serum gastrin level was observed in 8 cases. Either achlorhydria or marked hypoacidity was found in 6 cases with the level more than 400 pg/ml. The HCl administration temporarily lowered elevated gastrin levels, and feedback inhibition by HCl was found to be maintained. A rise in gastric pH was considered to be one of the prerequisites for an increase in serum gastrin level.
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PMID:Gastric acid secretion, serum gastrin and parietal cell histology in hyperthyroidism. 707 32

Infection by viral or bacterial pathogens has been suspected in playing a role in the development of autoimmune thyroid disease. Because Helicobacter pylori might be involved in the development of nongastrointestinal conditions such as rosacea, ischemic heart disease, and diabetes mellitus, we evaluated the prevalence of H. pylori infection in patients with autoimmune thyroid disease. Fifty-nine patients with autoimmune thyroid disease were included: autoimmune atrophic thyroiditis (n=21), Hashimoto's thyroiditis (n=18), and Graves' disease (n=20). Twenty patients with nontoxic multinodular goiter served as controls for nonautoimmune thyroid disease, and 11 patients with Addison's disease served as controls for nonthyroid endocrine autoimmune disease. The levels of anti-H. pylori immunoglobulin G (IgG) were determined, and a radiolabeled urea breath test were performed. The prevalence of H. pylori infection was markedly increased in the patients with autoimmune atrophic thyroiditis (85.7%), compared with the controls with nontoxic multinodular goiter (40%) and Addison's disease (45.4%). Infection by H. pylori resulted in increased levels of gastrin, pepsinogen I, and pepsinogen II in the H. pylori-positive groups, compared with the H. pylori-negative groups. A positive linear regression was found between the levels of microsomal autoantibodies and those of anti-H. pylori IgG in patients with autoimmune atrophic thyroiditis (n=21; r=0.79; p < 0.01). Finally, and although the overall prevalence of H. pylori infection was not increased, the anti-H. pylori IgG levels and the results from the breath test were higher in the patients with Graves' disease and Hashimoto's thyroiditis patients than in the controls. Clearly, the prevalence of H. pylori infection is increased in autoimmune atrophic thyroiditis and results in abnormalities of gastric secretory function. The strong relation between the levels of anti-H. pylori IgG and the levels of microsomal antibodies suggests that H. pylori antigens might be involved in the development of autoimmune atrophic thyroiditis or that autoimmune function in autoimmune atrophic thyroiditis may increase the likelihood of H. pylori infection.
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PMID:Helicobacter pylori infection is markedly increased in patients with autoimmune atrophic thyroiditis. 964 6

The present study was designed to evaluate the anti-ulcerogenic properties of an alkaloid chromane, rohitukine from Dysoxylum binectariferum. Anti-ulcer potential of rohitukine was assessed in cold restrained, pyloric ligated and ethanol induced ulcers in rats. In addition, rohitukine was tested in vitro for H(+) K(+)-ATPase inhibitory activity in gastric microsomes. Moreover, we studied the role of rohitukine on the cytosolic concentration of Ca(2+) in parietal cell-enriched cell suspension in order to ascertain its mechanism of action. Cytoprotective activity was evaluated through PGE(2) level. Rohitukine significantly attenuated the ulcers in cold restraint ulcer (CRU) model in a dose-related manner. Moreover, it significantly lowered the free acidity and pepsin activity in pyloric ligated rats while improved the depleted level of mucin. Furthermore, rohitukine significantly reversed the cold restrained-induced increase in gastrin level. Our in vitro study revealed that rohitukine moderately inhibited the microsomal H(+) K(+)-ATPase activity with respect to positive control omeprazole. Furthermore, rohitukine potently antagonized the gastrin-elicited increase in cytosolic Ca(2+) level in parietal cell-enriched suspension. In ethanol-induced gastric lesions in rats, rohitukine significantly inhibited the formation of erosions and increased PGE(2) content showing more potency than reference drug sucralfate. Our results thus suggest that rohitukine possess significant anti-ulcer and anti-gastrinic activity in rats. It is likely that gastro-protective influences of rohitukine are dependent partly on its acid-lowering potential and partly on cytoprotective property. The acid-reducing effect of rohitukine might be attributed to its lowering effect on gastrin production and/or antagonism of gastrin-evoked functional responses of parietal cells. Thus, rohitukine represent a useful agent in the treatment of peptic ulcer disease.
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PMID:Gastroprotective effect of anti-cancer compound rohitukine: possible role of gastrin antagonism and H(+) K (+)-ATPase inhibition. 2211 19