| Project/Area Number |
02454234
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
SUMII Koji University Medial Hospital Hiroshima University Assistant Professor, 医学部附属病院, 講師 (00116609)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIHARA Masaharu Hiroshima University School of Medicine Research Associate, 医学部, 助手 (20211659)
KAJIYAMA Goro Hiroshima University School of Medicine Professor, 医学部, 教授 (40034087)
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| Project Period (FY) |
1990 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥6,000,000 (Direct Cost: ¥6,000,000)
Fiscal Year 1992: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1991: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1990: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Keywords | Gut hormone / Somatostatin / Gastrin / GRP / H^+K^+-ATPase / mRNA / Duodenal ulcer / H^+K^+ATPase / 十二指腸漬瘍 / HKATPase |
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| Research Abstract |
1)Gene expression of gastrin and somatostatin in eating and fasting
Gastrin mRNA increased following eating and decreased during fasting. Mucosal somatostatin content and mRNA decreased after postprandial temporal increase, and gradually increased during fasting. These results indicated that somatostatin gene expression and storage of somatostatin to prepare the release of somatostatin to inhibit the acid and gastrin release following eating were important mechanism during fasting.
2)The role of GRP on gastrin release in PPI induced achlorhydria
We found a temporal increase of serum GRP level before increase of serum gastrin by PPI. Mucosal content of GRP depleted and recovered gradually, but GRPmRNA did not changed. Our results indicated that GRP mediate the PPI induced gastrin release in its initial stage.
3)Regulation of HK-ATPase mRNA
HK-ATPase mRNA was increased by PPI induced hypergastrinemia but it was not increased by H2-blocker induced hypergastrinemia, and the increase of HK-ATPase mRNA induced by PPI was inhibited by H2-blocker. These results indicated that gastrin stimulated the release of histamine from ECL-cell and then histamine stimulate HK-ATPase mRNA synthesis through H2-receptor.
4)Studies in peptic ulcer
Organ culture of antral mucosa, in which neurohumoral influences were excluded, revealed that the release and synthesis of gastrin were increased and those of somatostatin were decreased in patients with duodenal ulcer. Gastrin mRNA was increased by PPI but somatostatin mRNA did not changed in human.
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