| Project/Area Number |
15K18876
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pharmacology in pharmacy
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| Research Institution | Hokkaido Pharmaceutical University School of Pharmacy |
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Principal Investigator |
Takaguri Akira 北海道薬科大学, 薬学部, 准教授 (90623710)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | インスリン抵抗性 / ADAM17 / GIPC1 / 骨格筋細胞 / 小胞体ストレス / insulin resistance / skeletal muscle cells / AngiotensinII / IRS-1 / AMAM17 / ERK / ER stress / Insulin signaling / Yeast two-hybrid |
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| Outline of Final Research Achievements |
Inhibition of insulin signal transduction in skeletal muscle cell contributes to the development of type 2 diabetes. In this study, we investigated the role of a disintegrin and metalloprotease (ADAM) 17 in insulin signal transduction in skeletal muscle. Firstly, we found that ER stress induced by tunicamycin inhibits insulin signal transduction through the ADAM17 activation. Secondary, we found that GIPC1, a binding partner for ADAM17, is involved in angiotensin II-induced insulin resistance. Collectively, these data suggest that ADAM17 play a crucial role in regulation of insulin signal transduction.
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