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Miranda-Cervantes, A.* ; Fritzen, A.M.* ; Raun, S.H.* ; Hodek, O.* ; Møller, L.L.V.* ; Johann, K.* ; Deisen, L.* ; Gregorevic, P.* ; Gudiksen, A.* ; Artati, A. ; Adamski, J. ; Andersen, N.R.* ; Sigvardsen, C.M.* ; Carl, C.S.* ; Voldstedlund, C.T.* ; Kjøbsted, R.* ; Hauck, S.M. ; Schjerling, P.* ; Jensen, T.E.* ; Cebrian Serrano, A. ; Jähnert, M.* ; Gottmann, P.* ; Burtscher, I. ; Lickert, H. ; Pilegaard, H.* ; Schürmann, A.* ; Tschöp, M.H. ; Moritz, T.* ; Müller, T.D. ; Sylow, L.* ; Kiens, B.* ; Richter, E.A.* ; Kleinert, M.

Pantothenate kinase 4 controls skeletal muscle substrate metabolism.

Nat. Commun. 16:345 (2025)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Metabolic flexibility in skeletal muscle is essential for maintaining healthy glucose and lipid metabolism, and its dysfunction is closely linked to metabolic diseases. Exercise enhances metabolic flexibility, making it an important tool for discovering mechanisms that promote metabolic health. Here we show that pantothenate kinase 4 (PanK4) is a new conserved exercise target with high abundance in muscle. Muscle-specific deletion of PanK4 impairs fatty acid oxidation which is related to higher intramuscular acetyl-CoA and malonyl-CoA levels. Elevated acetyl-CoA levels persist regardless of feeding state and are associated with whole-body glucose intolerance, reduced insulin-stimulated glucose uptake in glycolytic muscle, and impaired glucose uptake during exercise. Conversely, increasing PanK4 levels in glycolytic muscle lowers acetyl-CoA and enhances glucose uptake. Our findings highlight PanK4 as an important regulator of acetyl-CoA levels, playing a key role in both muscle lipid and glucose metabolism.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Stimulated Glucose-transport; Insulin-resistance; Malonyl-coa; Exercise; Coenzyme; Ampk; Inflammation; Oxidation; Proteome; Reveals
Sprache englisch
Veröffentlichungsjahr 2025
HGF-Berichtsjahr 2025
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 16, Heft: 1, Seiten: , Artikelnummer: 345 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)
CF Metabolomics & Proteomics (CF-MPC)
Institute of Experimental Genetics (IEG)
Institute of Diabetes and Regeneration Research (IDR)
POF Topic(s) 30201 - Metabolic Health
30505 - New Technologies for Biomedical Discoveries
30203 - Molecular Targets and Therapies
90000 - German Center for Diabetes Research
Forschungsfeld(er) Helmholtz Diabetes Center
Enabling and Novel Technologies
Genetics and Epidemiology
PSP-Element(e) G-502200-001
A-630710-001
G-500600-001
G-505700-001
G-502300-001
G-501900-221
Förderungen Deutsche Forschungsgemeinschaft (DFG)
Danish Diabetes Academy
Novo Nordisk Foundation
Independent Research Fund Denmark
Lundbeck Foundation
National Health and Medical Research Council of Australia
German Research Foundation
German Center for Diabetes Research
European Research Council
Danish Council for Independent Research, Medical Sciences
Novo Nordisk Fonden (Novo Nordisk Foundation)
DOI 10.1038/s41467-024-55036-w
WOS ID 001390137100022
Scopus ID 85214470037
PubMed ID 39746949
Erfassungsdatum 2025-03-17
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