| Project/Area Number |
16590639
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Tokyo Women's Medical University |
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Principal Investigator |
SAITOH Toshihito Tokyo Women's Medical University, Dept.Internal Medicine, Assistant professor, 医学部, 講師 (50246609)
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| Co-Investigator(Kenkyū-buntansha) |
OHTUKA Hiroko Tokyo Women's Medical University, Dept.Internal Medicine, Assistant professor, 医学部, 助手 (20307606)
TAKAHASHI Haruki Tokyo Women's Medical University, Dept.Internal Medicine, Assistant professor, 医学部, 助手 (00246612)
FUKUSHIMA Yasushi University of Tokyo, Dept.Internal Medicine, Resident, 医学部, 医員
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2004: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | hypergastrinemia / histamine H2 receptor knock out mouse / gastric acidity / gastrin releasing cell / parital cell / ヒスタミン2受容体欠損マウス / 胃酸分泌抑制療法 / 胃内pHモニタリング |
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| Research Abstract |
It is well known that gastrin release from the antral G cell is regulated through the direct chemical effect of H+. Hypergastrinemia is induced by the suppression of gastric acid secretion using acid suppressants such as H2 receptor antagonists and proton pump inhibitors. However, the exact mechanism of regulating gastrin release has not been understood. We conducted the experiments to examine the relation of gastric acidity and gastrin release in histamine H2 receptor deficient mouse. We made gastric fistula in histamine H2 receptor deficient and wild type mice. We were able to perform 24 pH monitoring and change gastric pH by acid administration through gastric fistula in both mice. We found that the blood gastrin level varied with the changes of gastric pH in wild type mice. In histamine H2 receptor deficient mice, blood gastrin level was not influenced by the change of gastric pH. These results shown the possibility that gastrin release is stimulated by some signal transduction between parietal cells and gastsrin releasing cells. Therefore we are now planning for searching the candidate protein which possesses such signal transduction function. For this purpose, we performed an expression screening of mRNA derived from each portion of gastric mucosa. We tried to find out mRNA which shows an elevated expression when gastric pH increases.
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