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2014 Fiscal Year Final Research Report

Study on the role of metalloprotease ADAM in insulin signaling

Research Project

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Project/Area Number 25860064
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Pharmacology in pharmacy
Research InstitutionHokkaido 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
KeywordsADAM17 / 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.

Free Research Field

薬理学

URL: 

Published: 2016-06-03  

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