Amylin (islet amyloid polypeptide) is a hormone with suggested roles in the regulation of glucose homeostasis, gastric motor and secretory function and gastroprotection. In the gastric mucosa amylin is found co-localised with somatostatin in D-cells. The factors regulating gastric amylin release are unknown. In this study we have investigated the regulation of amylin release from gastric mucosal cells in primary culture. Rabbit fundic mucosal cells enriched for D-cells by counterflow elutriation were cultured for 40 hours. Amylin and somatostatin release over 2 hours in response to agonists were assessed.

A 25-year-old woman presented in April, 1998, with a 6-month history of epigastric pain with profuse watery diarrhoea. She had profuse haematemesis and was transfused with 6 units of blood. Endoscopy showed a post-bulbar duodenal ulcer. Serology and urea breath tests for Helicobacter pylori were negative. A proton pump inhibitor (PPI) was started. After 12 weeks of treatment, her symptoms had disappeared and the ulcer had healed. Her doctors made several attempts to withdraw PPI therapy over the following year, all of which caused recurrent symptoms. Additional tests were done at the end of 1999; plasma gastrin concentrations were raised at 400 pmol/L (NR: 20–100). Urinary excretion of catecholamines and 5-hydoxy-indole acetic acid were normal. Her doctors suspected that she had a gastrinoma and replaced the PPI by an H2-antagonist and sucralfate, planning to do a secretin provocation test. Before the test could be done she was readmitted with a perforated duodenal ulcer. The ulcer was surgically repaired and the PPI started again. Following the operation, the patient was noted to have a raised plasma calcium of 2·96 mmol/L (NR: 1·9–2·5) and raised parathormone of 210 ng/L (NR: 5–70). A parathyroid scan with 123I and technetium sestamibi showed increased uptake in the right lower gland. Her doctors thought that she probably had a parathyroid adenoma and started biphosphonates. On further questioning, the patient said that her father had a history of hypercalcaemia and an irresectable pancreatic tumour. The patient was transferred to our hospital for further tests.

BACKGROUND & AIMS Neuronal nitric oxide synthase (nNOS) is present in gastric D-cells. Mucosal somatostatin is diminished in H. pylori gastritis, where production of nitric oxide (NO) is increased. Therefore, we investigated the role of NO in D-cell function and the effects of prolonged exposure of D-cells to NO. METHODS Rabbit gastric D-cells were cultured. Somatostatin-14 was measured after 2 hours to examine the effects of arginine, nitric oxide sythase (NOS) inhibitors, and NO donors. Some cells were preincubated with a slow releasing NO donor for 12 hours. Results are expressed as percentage of total cell content. Nitrate content was measured by chemiluminescent assay. RESULTS L-arginine increased somatostatin-14 release in the presence of CCK8 from 4.4% +/- 0.5% to 6.4% +/- 0.4% (P < 0.02), and this was accompanied by NO release from 27 +/- 7 micromol/L to 86 +/- 12 micromol/L (P = 0.001). D-arginine and L-lysine had no effect. NOS inhibitors LNNA, SMT, and 7NI significantly attenuated the stimulatory response to L-arginine. NO donors sodium nitroprusside (SNP), 1 mmol/L, and S-nitroso-N-acetyl-D-L-penicillamine, 0.1 mmol/L, significantly increased basal and cholecystokinin-8 (CCK8) stimulated somatostatin release. Oxyhemoglobin attenuated the effect of SNP but not of L-arginine. Neither cyclic guanosine monophosphate nor guanylate cyclase were involved in the response to NO. However, inhibition of adenosine diphosphate (ADP) ribosyltransferase significantly decreased the response to L-arginine. Preincubation for 12 hours with 150 micromol/L (Z)-1-[(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate; IP3, inositol triphosphate decreased the 2-hour cellular response to CCK8 and SNP. CONCLUSIONS NO regulates rabbit D-cells. Acute exposure stimulates somatostatin mediated by ADP ribosylation, whereas long-term exposure reduces cellular responses to stimuli. The latter pathway may be responsible for the suppression of somatostatin in H. pylori gastritis.

OBJECTIVE:To investigate the mechanisms underlying the hypergastrinaemia of Helicobacter pylori by examining the effects of H. pylori on basal and stimulated gastrin release from cultured canine G-cells. METHODS:Canine antral G-cells were prepared by collagenase-EDTA digestion and cultured for 40 h. G-cells were then cultured for a further 24 h with two different H. pylori sonicates before basal and bombesin-stimulated gastrin release were measured by radioimmunoassay. RESULTS:Treatment of G-cells with both H. pylori sonicates significantly enhanced basal gastrin release (by 17-27%) and bombesin-stimulated gastrin release (by 115-133%). This effect was independent of cagA and vacuolating cytotoxin status. Control treatment with Escherichia coli sonicate had no effect on gastrin release. There was no change in the cellular content of gastrin. CONCLUSIONS:Incubation of antral G-cells with H. pylori constituents enhances subsequent basal and bombesin-stimulated gastrin release. Direct contact between H. pylori and G-cells in the gastric antrum may be responsible for the hypergastrinaemia seen with the infection.

ABSTRACT The relationship of Helicobacter felis, a bacterium observed in the stomachs of cats, to gastric disease is unclear. The objective of this study was to determine if H. felisinfection alters gastric histopathology, proinflammatory cytokine expression, and secretory function and evokes a humoral immune response in cats. Five specific-pathogen-free (SPF)Helicobacter-free cats were studied before and for 1 year after oral inoculation with H. felis (ATCC 49179). Four SPFH. felis-uninfected cats served as controls. The stomachs of all five H. felis-inoculated cats became colonized, as determined by urease activity, histopathology, PCR, culture, and transmission electron microscopy of serial gastric biopsies at 0, 3, 5, 8, and 12 months. Uninoculated cats remained Helicobacterfree. Lymphoid follicular hyperplasia, atrophy, and fibrosis were observed primarily in the pylorus of infected cats. Mild mononuclear inflammation was detected in both infected and uninfected cats, but was more extensive in infected cats, with pangastric inflammation, eosinophilic infiltrates, and cardia gastritis observed only in infected cats. No upregulation of antral mucosal interleukin 1α (IL-1α), IL-1β, or tumor necrosis factor alpha was detected by reverse transcription-PCR in any cat. The gastric secretory axes, assessed by fasting plasma gastrin, antral mucosal gastrin and somatostatin immunoreactivity, and pentagastrin-stimulated gastric acid secretion, were similar in both infected and uninfected cats. Gradual seroconversion (immunoglobulin G) was observed in four of five infected cats, with enzyme-linked immunosorbent assay values reaching 4× to 12× baseline 12 months postinfection. These findings indicate thatH. felis infection in cats induces lymphoid follicular hyperplasia, mild gastritis, and seroconversion, but is associated with normal gastric secretory function.

(2000) Am J Med 108, 65. Jackson JL, O'Malley PG, Tomkins G, et al. . Treatment of functional gastrointestinal disorders with antidepressant medications: a meta-analysis. . Jan; . : . –72 . [OpenUrl][1][CrossRef][2][PubMed][3][Web of Science][4] QUESTION: Are antidepressive agents efficacious for treating patients with functional gastrointestinal (GI) disorders? Studies were identified by searching Medline (1966–98), PsycLIT (1974–98), EMBASE/Excerpta Medica (1974–98), the Cochrane Library , and the Federal Research in Progress database using the terms antidepressive agents, serotonin reuptake inhibitors, monoamine oxidase inhibitors, amoxapine, clomipramine, tramipramine, desipramine, doxepin, imipramine, amitriptyline, maprotiline, nortriptyline, protriptyline, trazodone, nefazodone, fluoxetine, fluvoxamine, paroxetine, sertraline, femosetine, venlafaxine, bupropion, citalopram, mianserin, pizotyline, pizotifen, functional colonic diseases, dyspepsia, and abdominal pain. Bibliographies of relevant reviews and studies were scanned. Randomised controlled trials were selected if they compared an antidepressive agent with placebo in an adult population and outcome data were provided. Data were extracted on … [1]: {openurl}?query=rft.jtitle%253DThe%2BAmerican%2Bjournal%2Bof%2Bmedicine%26rft.stitle%253DAm%2BJ%2BMed%26rft.aulast%253DJackson%26rft.auinit1%253DJ.%2BL.%26rft.volume%253D108%26rft.issue%253D1%26rft.spage%253D65%26rft.epage%253D72%26rft.atitle%253DTreatment%2Bof%2Bfunctional%2Bgastrointestinal%2Bdisorders%2Bwith%2Bantidepressant%2Bmedications%253A%2Ba%2Bmeta-analysis.%26rft_id%253Dinfo%253Adoi%252F10.1016%252FS0002-9343%252899%252900299-5%26rft_id%253Dinfo%253Apmid%252F11059442%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [2]: /lookup/external-ref?access_num=10.1016/S0002-9343(99)00299-5&link_type=DOI [3]: /lookup/external-ref?access_num=11059442&link_type=MED&atom=%2Febmed%2F5%2F4%2F115.atom [4]: /lookup/external-ref?access_num=000084710800010&link_type=ISI

Conference Abstract| February 01 1999 Nitric Oxide Releases Somatostatin from Gastric D-Cells in Rabbit Primary Cell Culture N Arebi; N Arebi 1Department of Gastroenterology, Imperial College School of Medicine (Hammersmith Campus), Du Cane Road, London W12 ONN, England Search for other works by this author on: This Site PubMed Google Scholar ZV Healey; ZV Healey 1Department of Gastroenterology, Imperial College School of Medicine (Hammersmith Campus), Du Cane Road, London W12 ONN, England Search for other works by this author on: This Site PubMed Google Scholar PW Bliss; PW Bliss 1Department of Gastroenterology, Imperial College School of Medicine (Hammersmith Campus), Du Cane Road, London W12 ONN, England Search for other works by this author on: This Site PubMed Google Scholar M Ghatei; M Ghatei *Department of Metabolic Medicine, Imperial College School of Medicine (Hammersmith Campus), Du Cane Road, London W12 ONN, England Search for other works by this author on: This Site PubMed Google Scholar J Calam J Calam 1Department of Gastroenterology, Imperial College School of Medicine (Hammersmith Campus), Du Cane Road, London W12 ONN, England Search for other works by this author on: This Site PubMed Google Scholar Clin Sci (Lond) (1999) 96 (s40): 6P. https://doi.org/10.1042/cs096006P Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation N Arebi, ZV Healey, PW Bliss, M Ghatei, J Calam; Nitric Oxide Releases Somatostatin from Gastric D-Cells in Rabbit Primary Cell Culture. Clin Sci (Lond) 1 February 1999; 96 (s40): 6P. doi: https://doi.org/10.1042/cs096006P Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 1999 The Biochemical Society and the Medical Research Society1999 Article PDF first page preview Close Modal You do not currently have access to this content.

Source Citation Embil JM, Choudhri SH, Smart G, et al. Comparison of salivary and serum enzyme immunoassays for the diagnosis of Helicobacter pylori infection. Can J Infect Dis. 1998 Sep/Oct; 9:277-80.

Source Citation Labenz J, Blum AL, Bayerdorffer E, et al. Curing Helicobacter pylori infection in patients with duodenal ulcer may provoke reflux esophagitis. Gastroenterology. 1997 May;112:1442-7.

It has been exciting to witness the discovery that most peptic ulcers are caused by a bacterium that is relatively easy to eradicate. Most doctors now aim to give their patients the benefits of this u