2007 Fiscal Year Final Research Report Summary
Molecular Biological Analysis of Insulin Action
| Project/Area Number |
18590980
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 | University of Toyama |
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Principal Investigator |
ISHIKI Manabu University of Toyama, Graduate School of Medicine and Pharmaceutical Sciences for Research, Associate Professor (10422627)
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| Project Period (FY) |
2006 – 2007
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| Keywords | Diabetes Mellitus / Insulin Resistance / Signaling pathway / Glucose transporter / Actin filament / Microtubule |
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| Research Abstract |
Insulin regulates glucose uptake into the insulin target tissue in various mechanism. Especially, Glucose transporter 4, Glut4, plays a important final role for glucose uptake upon insulin stimulation. It translocates towards cell periphery, docks and is inserted into the plasma membrane so that glucose flows into the cell. It has been reported that actin filament which forms cell shape properly is facilitated Glut4 movement as well as signal input induced by insulin. Furthermore, microtubule is responsible for Glut4 traveling as well, although which regulators is more important still unsolved problem.
Here we show that actin filament appears to involve Glut4 translocation with class 1A PI3kinase signal input, whereas microtubule dependent Glut 4 translocation utilizes non-class 1A PI3klinase signal input by insulin stimulation. Interestingly, transferrin receptor movement towards cell periphery induced by insulin appears to share the same mechanism as Glut4 translocation which utilizes microtubules. Theses results indicate disturbance of ether two arms, one is actinfilament-class 1API3kinase dependent and the other is microtubule-non class 1A PI3kiasen dependent pathway, could cause a insulin resistance and type 2 diabetes mellitus so that to exploring the function of there arms in vivo would lead a new development of the ways of treatment of disease.
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