| Project/Area Number |
10557019
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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 |
Pathological medical chemistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
EBINA Yousuke The University of Tokushima, Institute for Enzyme Research, Professor, 分子酵素学研究センター, 教授 (00112227)
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| Co-Investigator(Kenkyū-buntansha) |
ASAHI Yoshihiko Otsuka Pharmaceutical Co., Ltd. Tokushima Institute, 分子酵素学研究センター, 研究員
YUASA Tomoyuki The University of Tokushima, Institute for Enzyme Research, Research Associate, 分子酵素学研究センター, 助手 (50304556)
KISHI Kazuhiro The University of Tokushima, Institute for Enzyme Research, Associate Professor, 分子酵素学研究センター, 助教授 (70284320)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥13,100,000 (Direct Cost: ¥13,100,000)
Fiscal Year 2000: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1999: ¥4,500,000 (Direct Cost: ¥4,500,000)
Fiscal Year 1998: ¥5,600,000 (Direct Cost: ¥5,600,000)
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| Keywords | Type 2 diabetes / Serumsubstance caused for insulin resistance / インスリン抵抗性 / NIDDM / トランスジェニックラット / GLUT4myc / インスリン非依存型糖尿病 |
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| Research Abstract |
NIDDM is primarily caused by the insulin resistance, and increase insulin secretion from pancreatic β-cells and sub-sequently deficiency of insulin. Therefore it is a key to find a substance for insulin resistance in the blood of the patient. There are several substrates in the plasma for insulin resistance, TGF-β, leptin and resistine. However, they are uncertain for insulin resistance of the onset of NIDDM.
Translocation of the type 4 glucose transporter (GLUT4) to the cell surface from an intracellular pool is the major mechanism of insulin-stimulated glucose uptake in insulin-target cells which is one of the most important physiological effect of insulin. We developed a highly sensitive and quantitative method to detect GLUT4 immunologically on the surface of intact cells, using c-myc epitope-tagged GLUT4 (GLUT4myc). We established stable clones to express GLUT4myc in 3T3L1 adipocytes and established the transgenic rat expressing GLUT4myc in rat adipocytes. We have developed a simple and new method to screen the compounds for triggering the GLUT4myc translocation in 96 wells using luminescence method. This method is useful for the first screening for finding the substances for insulin resistance. Recently, we found a part of known molecule may be the substance for insulin resistance.
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