2001 Fiscal Year Final Research Report Summary
Molecular mechanism underlying the GLUT4 translocation and its abnormality in diabetes mellitus
| Project/Area Number |
12470224
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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 | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | The University of Tokyo |
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Principal Investigator |
ASANO Tomoichiro Faculty of Medicine, Research Associate, 医学部附属病院, 助手 (70242063)
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| Co-Investigator(Kenkyū-buntansha) |
SAKODA Hideyuki Asahi Life Foundation, Research fellow, 成人病研究所, 研究員
ANAI Motonobu Asahi Life Foundation, Research fellow, 成人病研究所, 研究員
KATAGIRI Hideki Faculty of Medicine, Medical Staff, 医学部附属病院, 医員
FUJISHIRO Midori Faculty of Medicine, Medical Staff, 医学部附属病院, 医員
ONISHI Yukiko Asahi Life Foundation, Research fellow, 成人病研究所, 研究員
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| Project Period (FY) |
2000 – 2001
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| Keywords | Insulin / diabetes mellitus / Akt / PI 3 - Kinase / Insulin resistance |
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| Research Abstract |
We demonstrated that the activation of PI 3-kinase is necessary for the translocation of GLUT4 to the plasma membrane, and showed that the overexpression of the active mutant of Akt located downstream of PI 3-kinase induced the increased glucose uptake, similarly as observed for insulin stimulation. Since Akt is involved in the insulin-induced glucose metabolisms, we screened the protein associated with Akt, using yeast-two hybrid system, and identified a novel 200kDa protein.
Furthermore, we constructed the system by which we can observe the association of IRS-protein and PI 3-kinase in an intact cell system. On the other hand, we investigated the molecular mechanisms of insulin resistance using various rodent models. An interesting finding is that the insulin-induced PI 3-kinase activation was markedly enhanced in the hypertensive rat models, despite the presence of insulin resistance.
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Research Products
(14 results)
