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Jin, S.* ; Wu, W.* ; Liu, S.* ; Wang, Y.* ; Huang, Q.* ; He, K.* ; Ni, Y.* ; Chen, K.* ; Huang, J.* ; Liu, L.* ; Dai, J.* ; Zhan, C.* ; Wang, X.* ; Guan, Y.* ; Blüher, M.

Secreted EMC10 inhibits muscle GLUT4 activity and glucose uptake in mice.

J. Biol. Chem. 301:110296 (2025)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Manipulation of glucose uptake plays a critical role in muscle glucose disposal. We have shown that the secreted isoform of endoplasmic reticulum membrane protein complex subunit 10 (scEMC10) impairs glucose tolerance in mice and serum scEMC10 is positively associated with insulin resistance and hyperglycemia in humans. In this study, we attempt to investigate whether modulation of muscle glucose uptake implicates in the scEMC10-impacted glucose homeostasis. In mouse models, Emc10 gene knockout elevated, while recombinant scEMC10 treatment reduced, muscle glucose uptake and GLUT4 expression. In myoblasts, scEMC10 inhibited both GLUT4 expression and membrane translocation, and downregulated expression of genes associated with intracellular glucose metabolism. Mechanistically, scEMC10 suppressed the activation of muscle AMPK and insulin signaling cascades. Inhibition of scEMC10 via a neutralizing antibody enhanced muscle glucose uptake in mice, in parallel with heightened GLUT4 expression and membrane translocation, which accounts for an improved whole-body glucose homeostasis. In conclusion, this work identifies scEMC10 as a novel suppressor of muscle glucose uptake, and suggests inhibition of scEMC10 as a therapeutic strategy for type 2 diabetes.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Glut4 ; Glucose Uptake ; Secreted Emc10 ; Skeletal Muscle; Skeletal-muscle; Insulin-resistance; Ampk; Transport; Exercise; Translocation; Restoration; Expression; Cells; Ca2+
Sprache englisch
Veröffentlichungsjahr 2025
HGF-Berichtsjahr 2025
ISSN (print) / ISBN 0021-9258
e-ISSN 1083-351X
Zeitschrift Journal of Biological Chemistry, The
Quellenangaben Band: 301, Heft: 7, Seiten: , Artikelnummer: 110296 Supplement: ,
Verlag American Society for Biochemistry and Molecular Biology
Verlagsort Radarweg 29, 1043 Nx Amsterdam, Netherlands
Begutachtungsstatus Peer reviewed
Institut(e) Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
POF Topic(s) 30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-506501-001
Förderungen Science and Technology Commission of Shanghai Municipality
National Natural Science Foundation of China
DOI 10.1016/j.jbc.2025.110296
WOS ID 001517856000003
Scopus ID 105008286524
PubMed ID 40441535
Erfassungsdatum 2025-06-05
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