| Project/Area Number |
25461338
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | Nagoya University |
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Principal Investigator |
Yusuke Seino 名古屋大学, 医学(系)研究科(研究院), 特任助教 (80534833)
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| Co-Investigator(Kenkyū-buntansha) |
HAMADA Yoji 名古屋大学, 大学院医学研究科, 特任准教授 (20293706)
TSUNEKAWA Shin 名古屋大学, 医学部附属病院, 助教 (40612768)
OISO Yutaka 名古屋大学, 大学院医学研究科, 教授 (40203707)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | KATP channel / glucose / fructose / GIP / GLP-1 / SGLT1 / insulin / グルコース / フルクトース / ＫＡＴＰ ｃｈａｎｎｅｌ / SGLT-1 / ＧＩＰ / ＳＧＬＴ１ / ＧＬＰ－１ |
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| Outline of Final Research Achievements |
The KATP channel plays an essential role in glucose-induced insulin secretion from pancreatic beta-cells. KATP channels are also found in GIP-secreting K-cells, but, the physiological role of the KATP channels in K-cells is not known. We have clarified that (1)these KATP channels do not participate in GIP secretion under normoglycemic condition, (2)but contribute to glucose-induced GIP secretion under the streptozotocin-induced diabetic state, (3)fructose does not significantly stimulate GIP secretion in the normal state, but significantly enhances the GIP secretion in the streptozotocin-induced diabetic state, However, these KATP channels do not contribute to fructose-induced GIP secretion under hyperglycemic condition, and (4)while the expression levels of sodium-glucose co-transporter 1(SGLT1) mRNA in duodenum are increased by chronic loading of high-carbohydrate diet in mice, the KATP channels do not participate in this.
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