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

The present study was performed in order to evaluate: (1) the influence of a bicarbonate-alkaline mineral water (Uliveto) on digestive symptoms in patients with functional dyspepsia; (2) the effects of Uliveto on preclinical models of gastric functions. Selected patients complained of dyspeptic symptoms in the absence of digestive lesions or Helicobacter pylori infection within the previous 3 months. They were treated with Uliveto water (1.5 l day(-1)) for 30 days. Frequency and severity of symptoms were assessed at baseline and day 30 by a score system. Preclinical experiments were carried out on rats, allowed to drink Uliveto or oligomineral water for 30 days. Animals then underwent pylorus ligation to evaluate gastric secretion of acid, pepsinogen, and mucus. In separate experiments, gastric emptying was assessed. Crenotherapy was associated with a relief of epigastric pain, retrosternal pyrosis, postprandial fullness and gastric distention. At preclinical level, Uliveto water increased acid and pepsinogen secretions as well as gastric emptying, without changes in bound mucus. The enhancing actions of Uliveto on gastric secretions and emptying were prevented by L-365,260, an antagonist of gastrin/CCK-2 receptors. These findings indicate that a regular intake of Uliveto favors an improvement of dyspeptic symptoms. The preclinical study suggests that the clinical actions of Uliveto water depend mainly on its ability to enhance gastric motor and secretory functions.
 ...
PMID:Effects of a bicarbonate-alkaline mineral water on gastric functions and functional dyspepsia: a preclinical and clinical study. 1245 26

Helicobacter pylori has been recognized as one of the most important factors that lead to chronic changes in the gastric mucosa. These changes have either direct or indirect impact on various intestinal hormones (gastrin, somatostatin, bombensin, cholecystokinin...) which regulate gastric secretion. Gastric secretion enhancement is mostly caused by higher concentration of serum gastrin. The mechanism in which the Helicobacter pylori infection influences the regulation of gastrin and other intestinal hormones is yet to be discovered. It is known that eradication of the Helicobacter pylori infection decreases serum gastrin concentration, thus decreasing gastric secretion and inflammatory changes of the gastric mucosa.
 ...
PMID:[Hormonal regulation of gastric secretion and Helicobacter pylori]. 1259 9

Previous studies from our group have shown that hypergastrinemia in mice can synergize with Helicobacter felis infection to induce gastric carcinoma. In addition, epidemiological evidence and a recent study with C57BL/6 mice have strongly suggested a link between a high-salt diet during Helicobacter pylori infection and the development of hypergastrinemia and preneoplastic gastric lesions. To address the possible relationship between the two cofactors (gastrin and salt) and whether H. pylori can also lead to gastric cancer in this model, we undertook a longitudinal study involving 86 INS-GAS mice. The mice were fed either a high-salt (7.5%) or basal (0.25%) diet, and half were infected with H. pylori. Necropsies at 5 and 7 months postinfection included histopathological examination, quantitative culturing for bacterial colonization levels, and serology to estimate the magnitude of the Th1 and Th2 systemic inflammatory responses. Lesions consistent with in situ and intramucosal carcinoma were seen in H. pylori-infected male mice only. There was a highly significant main effect for Helicobacter infection status for all fundic and antral lesion parameters (P < 0.0001), as well as significant interactions of infection status with diet for all of the fundic parameters (all P < 0.03), except intestinal metaplasia. In subsequent ANOVAs in which the data were limited to that from infected animals, there was a highly significant main effect for time, diet, and gender (all P < 0.02) on all of the corpus lesion parameters scored (inflammation, atrophy, hyperplasia, metaplasia, and dysplasia/neoplasia). In addition, gender interacted significantly with time (all P < 0.03), and. H. pylori colonization increased quantitatively over the course of the experiment but were independent of either diet or gender. The Th1-associated serum IgG2a responses to H. pylori increased from the time of experimental infection to necropsy at 5 or 7 months and were similar among all experimentally infected mice with no influence of gender (P > 0.10) or dietary salt (P > 0.27). In contrast, the Th2-associated serum IgG1 response to H. pylori was significantly increased in infected male INS-GAS mice on the high-salt diet at 7 months postinfection (P < 0.012). These results show that H. pylori can also accelerate the development of gastric cancer in the INS-GAS mouse model, and the results suggest that salt has less of a procarcinogenic effect in the setting of endogenous hypergastrinemia. The increased Th2-associated humoral response of the infected male mice on the high-salt diet correlated with less severe gastric lesions. In the INS-GAS mouse model, male gastric tissue responded more rapidly and aggressively to H. pylori infection, high-salt diet, and the combination when compared with females; a finding that appears consistent with the greater incidence of gastric carcinoma in men. This study highlights the importance of using both genders to investigate the pathogenesis of H. pylori.
 ...
PMID:Helicobacter pylori-associated gastric cancer in INS-GAS mice is gender specific. 1261 7

The gastric hormone gastrin is produced in multiple forms that vary in their biological properties. In this analytical review, the strategies available for the assay of different gastrins in plasma are considered. Except for research purposes, it is seldom necessary or even desirable to employ assays that are specific for an individual molecular form of gastrin. Instead, routine clinical assays of plasma gastrin should ideally react equally with the sulphated and unsulphated forms of the COOH-terminally amidated peptides, the most important of which are peptides of 17 and 34 amino acid residues (i.e. G17 and G34), and should not react with the related hormone cholecystokinin. Methods appropriate for the use of such assays are reviewed. These assays are important in the diagnosis of gastrinoma. Although it is recognized that circulating concentrations of gastrin are elevated in other conditions, including chronic atrophic gastritis, Helicobacter pylori infection and long-term administration of proton pump inhibitors, it is not clear whether gastrin radioimmunoassay is important for the clinical management in these conditions.
 ...
PMID:Gastrin: an analytical review. 1450 84

Fifty percent of the world's population is infected with Helicobacter pylori; however, treatment has been insufficient to eradicate the organisms due to rising antibiotic resistance. Helicobacter infection is characterized by induction of a T helper 1 lymphocyte (Th1) immune response, hypergastrinemia, and suppressed tissue somatostatin (SOM) levels. However, the mechanism by which the immune response regulates acid secretion is not known. We show here that treatment with IFN-gamma, a Th1 cytokine, was sufficient to induce gastritis, increase gastrin, and decrease SOM levels within 7 days. In contrast, the T helper 2 lymphocyte cytokine IL-4 increased SOM levels and effectively suppressed gastrin expression and secretion. This result demonstrated reciprocal regulation of acid regulatory peptides by immune modulators. IL-4 pretreatment prevented gastritis in infected wild-type but not in SOM null mice. Thus, the ability of IL-4 to oppose a Th1-mediated infection required SOM. Immunofluorescence was used to document the presence of IL-4 receptors on the gastric SOM-secreting cell (D cell). Moreover, IL-4 stimulated SOM release from primary D cell cultures. Treatment of mice chronically infected with Helicobacter felis for 2 mo with the SOM analogue octreotide resolved the inflammation. Thus, a mechanism by which IL-4 resolves inflammation in the stomach is by stimulating the release of SOM from gastric D cells.
 ...
PMID:Treatment of Helicobacter gastritis with IL-4 requires somatostatin. 1455 68

Helicobacter pylori infection is a causal factor of gastric cancer (which is associated with low gastric acid secretion) or duodenal ulcer (high acid secretion). Parietal cells and ECL cells in the stomach are controlled by gastrin, which plays a crucial role in the regulation of acid secretion. The present study was undertaken to identify a possible role of gastrin in determining the different responses of the parietal cells and ECL cells to chronic H. pylori infection. Wild-type (C57BL/6J) gastrin(+/+) mice and gastrin(-/-) knockout mice, generated through targeted gene disruption and backcrossed eight times to C57BL/6J, were infected with H. pylori for 9 months. The acid output was measured 4 h after pylorus ligation (known to cause vagal excitation). The gastric mucosa was examined by immunocytochemistry with antisera to alpha-subunit of H+/K(+)-ATPase for the parietal cells, and to histamine and vesicle monoamine transporter-2 for the ECL cells, and by quantitative electron microscopy. In infected gastrin(+/+) mice, the acid output and the percentage of secreting parietal cells (freely fed state) were 20-30% of the values in uninfected controls, while the density and ultrastructure of parietal cells were normal. The infected mice had hypergastrinemia and displayed hypertrophy and hyperplasia of ECL cells. Although uninfected gastrin(-/-) mice had lower the acid output than uninfected gastrin(+/+) mice, there was a higher acid output (approximately 3 times) in infected gastrin(-/-) mice than their uninfected homologues. The numbers of parietal cells and ECL cells remained unchanged in infected gastrin(-/-) mice. In conclusion, chronic H. pylori infection results to impaired parietal-cell function (acid hyposecretion), hypergastrinemia and hyperplasia of ECL cells in wild-type mice but leads to vagally induced hypersecretion in gastrin-deficient mice.
 ...
PMID:Chronic Helicobacter pylori infection results in gastric hypoacidity and hypergastrinemia in wild-type mice but vagally induced hypersecretion in gastrin-deficient mice. 1455 57

Gastric cancer is the second most common cause of cancer-related mortality world-wide. In most cases, it develops via the pre-malignant stages of atrophic gastritis, intestinal metaplasia and dysplasia, following Helicobacter pylori infection of susceptible individuals. A number of rodent models have recently provided valuable insights into the host, bacterial and environmental factors involved in gastric carcinogenesis. Wild-type rodents do not develop gastric adenocarcinoma, but early studies showed that the disease could be induced in several rodent species by chemical carcinogens. More recently, it has been demonstrated that gastric adenocarcinoma can be induced in Mongolian gerbils by H. pylori infection and in C57BL/6 mice by long-term H. felis infection. These models have allowed the importance of Helicobacter virulence genes, host factors, such as gender, strain and immune response, and environmental factors, such as dietary salt, to be explored. A number of transgenic mice with alterations in various pathways, including the immune response, gastrin biosynthesis, parietal cell development, growth factors and tumour suppressors, have also provided models of various stages of gastric carcinogenesis. One model that has proved to be particularly valuable is the hypergastrinaemic INS-GAS mouse, in which gastric carcinoma develops spontaneously in old animals, but the process is greatly accelerated by Helicobacter infection.
 ...
PMID:Review article: How useful are the rodent animal models of gastric adenocarcinoma? 1508 Aug 46

In 1984, Reg protein was shown to be stimulated during the regeneration of pancreatic islets. Since then, many Reg-related proteins have been identified in humans and other animals. These Reg-related proteins are classified into four subfamilies according to their amino-acid sequences, but they share a similar structure and physiological function. The role of Reg in gastric tissue was investigated, and Reg I was found to be expressed mainly in gastric fundic enterochromaffin-like (ECL) cells. Reg I production in ECL cells is stimulated by gastrin, as well as by the proinflammatory cytokine, cytokine-induced neutrophil chemoattractant (CINC)-2Beta. In patients with chronic hypergastrinemia, Reg production is stimulated, with the increased proliferation of gastric mucosal cells. Patients with Helicobacter pylori infection also showed increased Reg production in the gastric mucosa, partly via increased plasma gastrin concentration and partly via increased proinflammatory cytokine production. Thus, Reg protein induced by H. pylori infection may be partly responsible for the increased proliferation of gastric epithelial cells in H. pylori-infected patients. Reg protein is also produced in many gastric cancer cells, especially in poorly differentiated and advanced cancers. Reg protein stimulates the proliferation of several gastric cancer cell types, and gastric cancers with Reg protein expression tend to show a poorer clinical outcome. In summary, Reg protein may be a growth factor that regulates the proliferation and differentiation of normal and neoplastic gastric epithelial cells.
 ...
PMID:Reg protein is a unique growth factor of gastric mucosal cells. 1523 66

The gastrointestinal peptide hormones gastrin and cholecystokinin (CCK) are well known for their ability to stimulate gastric acid secretion and pancreatic enzyme secretion, respectively. The suggestion that gastrin and CCK might also promote the development of cancers of the gastrointestinal tract has been controversial, but an increasing body of evidence now supports the view that the amidated and non-amidated forms of gastrin act as growth factors via different receptors in different regions of the gut. For example, animal experiments indicate that amidated gastrins are involved in cellular differentiation and repair in the gastric mucosa, and synergize with Helicobacter pylori infection in the development of gastric carcinoma. In contrast, non-amidated gastrins stimulate colonic mucosal growth, accelerate the early steps in colorectal carcinoma formation, and are elevated in the tumour and circulation of patients with colorectal cancer. Although human pancreatic carcinomas express CCK-1 and CCK-2 receptors, the role of gastrins and CCK in pancreatic carcinogenesis is yet to be established. Further investigation of the possible role of the CCK-2 receptor in gastric and pancreatic neoplasia, and of the hypothesis that gastrin precursors act as autocrine growth factors in colorectal carcinoma, is warranted. However, therapies aimed at the gastrins must be targeted to the relevant gastrin/gastrin receptor combination.
 ...
PMID:Gastrins, cholecystokinins and gastrointestinal cancer. 1523 41

The aim of this study was to estimate the levels of serum gastrin in a group of patients with either ulcerative colitis or Crohn's disease and to compare the results with those of a group of normal controls. In 108 consecutive patients with IBD (66 with ulcerative colitis, 32 with Crohn's disease and 10 with indetermined colitis) serum levels of gastrin were measured by radioimmunoassay. One hundred and eight normal people were served as controls. The levels of serum gastrin were significantly elevated in patients with Crohn's disease compared to normal controls (74.4 +/- 43.9 pg/ml vs. 47.5 +/- 32.4 pg/ml, P<0.05), irrespectively of the activity of the disease. On the contrary, patients with ulcerative colitis exhibited no significant differences compared to normal controls. Differences between Crohn's disease and ulcerative colitis patients were statistically significant (P<0.001). The rate of infection by Helicobacter pylori in patients with inflammatory bowel disease was statistically significantly lower as compared with normal controls (31.7% vs. 55.1%, P<0.001). It is concluded that patients with active or inactive Crohn's disease have increased levels of serum gastrin. This may have implications concerning the high incidence of upper GI lesions found in patients with Crohn's disease despite the very low incidence of Helicobacter pylori infection.
 ...
PMID:Serum gastrin levels in patients with inflammatory bowel disease. 1524 13


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>