Pantothenate kinase 4 controls skeletal muscle substrate metabolism. 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. Nature Communications, 16(1):345, January, 2025. Publisher: Nature Publishing Group![Pantothenate kinase 4 controls skeletal muscle substrate metabolism [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex 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.
@article{miranda-cervantes_pantothenate_2025,
title = {Pantothenate kinase 4 controls skeletal muscle substrate metabolism},
volume = {16},
copyright = {2025 The Author(s)},
issn = {2041-1723},
url = {https://www.nature.com/articles/s41467-024-55036-w},
doi = {10.1038/s41467-024-55036-w},
abstract = {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.},
language = {en},
number = {1},
urldate = {2025-01-10},
journal = {Nature Communications},
author = {Miranda-Cervantes, Adriana and Fritzen, Andreas M. and Raun, Steffen H. and Hodek, Ondřej and Møller, Lisbeth L. V. and Johann, Kornelia and Deisen, Luisa and Gregorevic, Paul and Gudiksen, Anders and Artati, Anna and Adamski, Jerzy and Andersen, Nicoline R. and Sigvardsen, Casper M. and Carl, Christian S. and Voldstedlund, Christian T. and Kjøbsted, Rasmus and Hauck, Stefanie M. and Schjerling, Peter and Jensen, Thomas E. and Cebrian-Serrano, Alberto and Jähnert, Markus and Gottmann, Pascal and Burtscher, Ingo and Lickert, Heiko and Pilegaard, Henriette and Schürmann, Annette and Tschöp, Matthias H. and Moritz, Thomas and Müller, Timo D. and Sylow, Lykke and Kiens, Bente and Richter, Erik A. and Kleinert, Maximilian},
month = jan,
year = {2025},
note = {Publisher: Nature Publishing Group},
keywords = {Diabetes, Fat metabolism, Homeostasis, Metabolomics},
pages = {345},
}
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