| Project/Area Number |
09557101
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Digestive surgery
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| Research Institution | Tohoku University |
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Principal Investigator |
SASAKI Iwao Tohoku University Associate Professor, 医学部, 助教授 (60125557)
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| Co-Investigator(Kenkyū-buntansha) |
SASAKI Kazuyuki Tohoku University, 創薬研究所, 研究員
SASANO Kiminobu Tohoku University Professor, 医学部, 教授 (50187142)
FUKUSHIMA Kohei Tohoku University Research associate, 医学部, 助手 (20271900)
FUNAYAMA Yuji Tohoku University Lecturer, 医学部・附属病院, 講師 (50192315)
NAITO Hiroo Tohoku University Lecturer, 医学部・附属病院, 講師 (90180223)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥12,100,000 (Direct Cost: ¥12,100,000)
Fiscal Year 1998: ¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1997: ¥9,800,000 (Direct Cost: ¥9,800,000)
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| Keywords | total colectomy / QDL / hyperaldosteronism / 11betaHSD2 / ENaC / Na^+-K^+ ATPase / Ileo-jejunal transposition / Enteroglucagon / Peptide YY / 11B HSD2 / E NaC / Na^+-K^+ ATPase / ileo-jejunal transposition(IJT) / Peptide YY / 電解質吸収能 |
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| Research Abstract |
[In Rats] We examined function and gene induction relating to the function of aldosteron in small intestinal mucosa and kidney after total proctocolectomy(TPC). Adimnistration of aldosteron evoked amiloride-sensitive short circuit current(Isc) after TPC, otherwise no response of Isc was observed in normal rats. In lower small intestine, TPC induced the activation of 11beta hydroxysteroid dehydrogenase type 2(11beta HSD2) which regulates the function of aldosteron, and alpha, subunit mRNA of amiloride-sensitive epithelial Na+ channel(ENaC). In kidney, 1113 HSD2, alpha beta gamma subunit mRNA of ENaC, and a 1beta1 subunit mRNA of Na+-K+ ATPase were enhanced after TPC.We concluded that hyperaldosteronism is a very important mechanism for the regulation of water and electrolyte balance after total proctocolectomy.
[In dogs] Ileal brake, that upper gastrointestinal motility was suppressed by the infusion of nutrients(fat, glucose, etc) into the ileum, has been well recognized. We have conceived the model of Ileo-jejunal transposition(IJT) which is a possible operative procedure to modify this mechanism. We examined the effect of IJT on the motility and transit in normal or totally colectomized dogs. In normal dogs, IJT suppressed postprandial gastric motility and delayed gastric emptying. Plasma enteroglucagon(EG) and Peptide YY(PYY) level were increased in IJT group. In colectomized dogs, IJT delayed gastric emptying and reduced water content of the stool. We conclude that IJT may be a novel operative procedure, which can suppress the upper gastrointestinal motility and improve the quality of life in patients who received total proctocolectomy.
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