Ken Sugimoto
   Department   Kawasaki Medical School  Kawasaki Medical School, Department of General Geriatric Medicine,
   Position   Professor
Article types 原著
Language English
Peer review Peer reviewed
Title Overexpression of Interleukin-15 exhibits improved glucose tolerance and promotes GLUT4 translocation via AMP-Activated protein kinase pathway in skeletal muscle.
Journal Formal name:Biochemical and biophysical research communications
Abbreviation:Biochem Biophys Res Commun
ISSN code:10902104/0006291X
Domestic / ForeginForegin
Volume, Issue, Page 509(4),pp.994-1000
Author and coauthor Fujimoto Taku, Sugimoto Ken, Takahashi Toshimasa, Yasunobe Yukiko, Xie Keyu, Tanaka Minoru, Ohnishi Yuri, Yoshida Shino, Kurinami Hitomi, Akasaka Hiroshi, Takami Yoichi, Takeya Yasushi, Yamamoto Koichi, Rakugi Hiromi
Publication date 2019/02
Summary Skeletal muscle performs 80% of the glucose metabolism in the body. Improvement of insulin resistance and prevention of diabetes by habitual exercise is considered beneficial due to the improved glucose uptake in skeletal muscles. Investigation of the mechanism by which skeletal muscles regulate glucose uptake can contribute to the prevention and treatment of diabetes. Myokines are a kind of cytokine secreted from skeletal muscle, which are expected to regulate muscle metabolism. Interleukin-15 (IL-15) is one such myokine that has been reported to improve glucose metabolism in vitro, although the mechanism remains unclear. In this study, we examined the glucose metabolism of skeletal muscle-specific IL-15 transgenic mice (IL-15TG), and investigated how IL-15 affects glucose metabolism in skeletal muscles. Although High Fat Diet-fed IL-15TG did not exhibit obvious difference in intraperitoneal insulin tolerance test, they had less impaired glucose tolerance compared to wild-type C57BL/6. Phosphorylation of AMP-activated protein kinase (AMPK), Akt substrate of 160 kDa (AS160), tre-2/USP6, BUB2, and cdc16 domain family member 1 (TBC1D1), and translocation of Glucose transporter type 4 (GLUT4) were accelerated in the skeletal muscle of IL-15TG. Our study demonstrated that overexpression of IL-15 in skeletal muscle improves glucose metabolism in skeletal muscle via AMPK pathway. We report the first in-vivo study that describes the signaling pathway of IL-15 in muscle glucose metabolism, and thereby contributes to the elucidation of the regulatory mechanism of muscle glucose metabolism by myokines.
DOI 10.1016/j.bbrc.2019.01.024
PMID 30654941