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2022 Fiscal Year Final Research Report

Establishment and functional analysis of mouse cultured skeletal muscle clone cells lacking insulin 1 and 2

Research Project

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Project/Area Number 21K19725
Research Category

Grant-in-Aid for Challenging Research (Exploratory)

Allocation TypeMulti-year Fund
Review Section Medium-sized Section 59:Sports sciences, physical education, health sciences, and related fields
Research InstitutionTokyo Metropolitan University

Principal Investigator

FUJII Nobuharu  東京都立大学, 人間健康科学研究科, 教授 (40509296)

Project Period (FY) 2021-07-09 – 2023-03-31
Keywords骨格筋 / インスリン / 筋肥大 / 筋萎縮
Outline of Final Research Achievements

Our group has discovered that "insulin is also produced and secreted by skeletal muscle cells." Therefore, the aim of this study is to disrupt the two insulin genes in mice skeletal muscle cells to make them dysfunctional. It was knocked down by lentivirus or adeno-associated virus vector using the CRISPER-Cas9 method, but the infection efficiency of both vectors was low despite various improvements. However, when the genes knockdown by siRNA was attempted, highly efficient genome editing became possible.

Free Research Field

運動分子生物学

Academic Significance and Societal Importance of the Research Achievements

申請者はこれまでに、骨格筋から分泌されるホルモンの網羅的探索を進めてきた。その過程で、インスリンが骨格筋でも産生・分泌されている証拠を複数得た。骨格筋が、膵臓から分泌されるインスリンの単なる受け手ではなく、自身でもインスリンを産生・分泌しているとなれば、これまでの加齢性筋萎縮成立機序とその予防・治療法の常識は覆される。そこで本研究では、「骨格筋から分泌されるインスリンの変調がサルコペニアを誘起する」という仮説を検証することを目的とした。

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Published: 2024-01-30  

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