| Project/Area Number |
06454627
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
体育学
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| Research Institution | University of Tsukuba |
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Principal Investigator |
TOKUYAMA Kampei Institute of Health and Sport Science, University of Tsukuba Assistant Professor, 体育科学系, 講師 (00207565)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Masashige Institute of Health and Sport Science, University of Tsukuba Professor, 体育科学系, 教授 (90015842)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 1995: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1994: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | endurance training / diabetes / insulin receptor / IRS-1 / PI 3-kinase / GLUT 4 / GLUT4 / 糖尿病 / インシュリン受容体遺伝子 / 持久的運動 / 骨格筋 |
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| Research Abstract |
Endurance training enhances insulin sensitivity with increasing insulin receptor number in skeletal muscle. Insulin receptor exists in two isoforms, and the two isoforms possess distinct functional properties and are expressed in a tissue-specific fashion. Therefore, one recently evolved candidate mechanism for the regulation of insulin sensitvity is an altered expression pattern of the insulin receptor isoforms. When insulin receptor binds insulin, its tyrosine kinase phosphorylates insulin receptor itself and the insulin receptor substrate-1 (IRS-1). This multiple phosphorylation results in a non-covalent binding of the specific intracellular proteins such as phosphatidylinositol 3-kinase (PI 3-kinase) to IRS-1. Following the phosphorylation of IRS-1, some effect of insulin, such as increased glucose uptake, appear to be closely linked to the activation of PI 3 kinase. Insulin signaling pathways mediated through the activation of the IRS-1 and PI 3-kinase are therefore another potential sites for controlling insulin sensitivity.
In this study, we examined effects of endurance training on alternative splicing of insulin receptor mRNA and gene expression of insulin receptor, IRS-1 and PI 3-kinase in rat skeletal muscle. Our findings provide the first evidence that gene expression of insulin receptor and postreceptor signal transduction pathway (IRS-1 and PI 3-kinase) is enhanced by endurance training, without affecting alternative splicing of insulin receptor isoforms.
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