2014 Fiscal Year Final Research Report
Study on the role of metalloprotease ADAM in insulin signaling
Project/Area Number |
25860064
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Pharmacology in pharmacy
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Research Institution | Hokkaido Pharmaceutical University School of Pharmacy |
Principal Investigator |
TAKAGURI Akira 北海道薬科大学, 薬学部, 准教授 (90623710)
|
Project Period (FY) |
2013-04-01 – 2015-03-31
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Keywords | ADAM17 / Insulin signaling / Interluekin-1 / Endothelin-1 / Insulin resistance / Skeletal muscle cells |
Outline of Final Research Achievements |
Insulin resistance on skeletal muscle cells contributes to the pathogenesis of type 2 diabetes. In this study, we examined the role of a disintegrin and metalloprotease ADAM17 on insulin signal transduction in L6 myotubes. Interluekin-1 increases ADAM17 expression through the ERK/NFκB and JNK/AP-1 signaling pathways. We also observed that endothelin-1 significantly inhibited insulin-induced IRS-1 tyrosine phosphorylation and Akt phosphorylation when ADAM17 were over-expressed. These results suggest that ADAM17 expression plays a pivotal role in ET-1-impaired insulin signal transduction in L6 myotubes.
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Free Research Field |
薬理学
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