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The myokine meteorin-like (metrnl) improves glucose tolerance in both skeletal muscle cells and mice by targeting AMPK alpha 2

Authors
Lee, Jung OkByun, Won SeokKang, Min JuHan, Jeong AhMoon, JiyoungShin, Min-JeongLee, Ho JunChung, Ji HyungLee, Jin-SeokSon, Chang-GueSong, Kwon-HoKim, Tae WooLee, Eun-SooKim, Hong MinChung, Choon HeeNgoei, Kevin R. W.Ling, Naomi X. Y.Oakhill, Jonathan S.Galic, SandraMurray-Segal, LisaKemp, Bruce E.Kim, Kyoung MinLim, SooKim, Hyeon Soo
Issue Date
5월-2020
Publisher
WILEY
Keywords
adipomyokine; AMPK; glucose uptake; Metrnl; type 2 diabetes
Citation
FEBS JOURNAL, v.287, no.10, pp.2087 - 2104
Indexed
SCOPUS
Journal Title
FEBS JOURNAL
Volume
287
Number
10
Start Page
2087
End Page
2104
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/56191
DOI
10.1111/febs.15301
ISSN
1742-464X
Abstract
Meteorin-like (metrnl) is a recently identified adipomyokine that beneficially affects glucose metabolism; however, its underlying mechanism of action is not completely understood. We here show that the level of metrnl increases in vitro under electrical pulse stimulation and in vivo in exercised mice, suggesting that metrnl is secreted during muscle contractions. In addition, metrnl increases glucose uptake via the calcium-dependent AMPK alpha 2 pathway in skeletal muscle cells and increases the phosphorylation of HDAC5, a transcriptional repressor of GLUT4, in an AMPK alpha 2-dependent manner. Phosphorylated HDAC5 interacts with 14-3-3 proteins and sequesters them in the cytoplasm, resulting in the activation of GLUT4 transcription. An intraperitoneal injection of recombinant metrnl improved glucose tolerance in mice with high-fat-diet-induced obesity or type 2 diabetes, but not in AMPK beta 1 beta 2 muscle-specific null mice. Metrnl improves glucose metabolism via AMPK alpha 2 and is a promising therapeutic candidate for glucose-related diseases such as type 2 diabetes.
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