Impaired phosphocreatine metabolism in white adipocytes promotes inflammation. Maqdasy, S., Lecoutre, S., Renzi, G., Frendo-Cumbo, S., Rizo-Roca, D., Moritz, T., Juvany, M., Hodek, O., Gao, H., Couchet, M., Witting, M., Kerr, A., Bergo, M. O., Choudhury, R. P., Aouadi, M., Zierath, J. R., Krook, A., Mejhert, N., & Rydén, M. Nature Metabolism, 4(2):1–13, February, 2022. ![Impaired phosphocreatine metabolism in white adipocytes promotes inflammation [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex The mechanisms promoting disturbed white adipocyte function in obesity remain largely unclear. Herein, we integrate white adipose tissue (WAT) metabolomic and transcriptomic data from clinical cohorts and find that the WAT phosphocreatine/creatine ratio is increased and creatine kinase-B expression and activity is decreased in the obese state. In human in vitro and murine in vivo models, we demonstrate that decreased phosphocreatine metabolism in white adipocytes alters adenosine monophosphate-activated protein kinase activity via effects on adenosine triphosphate/adenosine diphosphate levels, independently of WAT beigeing. This disturbance promotes a pro-inflammatory profile characterized, in part, by increased chemokine (C-C motif) ligand 2 (CCL2) production. These data suggest that the phosphocreatine/creatine system links cellular energy shuttling with pro-inflammatory responses in human and murine white adipocytes. Our findings provide unexpected perspectives on the mechanisms driving WAT inflammation in obesity and may present avenues to target adipocyte dysfunction.
@article{maqdasy_impaired_2022,
title = {Impaired phosphocreatine metabolism in white adipocytes promotes inflammation},
volume = {4},
copyright = {2022 The Author(s)},
issn = {2522-5812},
url = {https://www.nature.com/articles/s42255-022-00525-9},
doi = {10.1038/s42255-022-00525-9},
abstract = {The mechanisms promoting disturbed white adipocyte function in obesity remain largely unclear. Herein, we integrate white adipose tissue (WAT) metabolomic and transcriptomic data from clinical cohorts and find that the WAT phosphocreatine/creatine ratio is increased and creatine kinase-B expression and activity is decreased in the obese state. In human in vitro and murine in vivo models, we demonstrate that decreased phosphocreatine metabolism in white adipocytes alters adenosine monophosphate-activated protein kinase activity via effects on adenosine triphosphate/adenosine diphosphate levels, independently of WAT beigeing. This disturbance promotes a pro-inflammatory profile characterized, in part, by increased chemokine (C-C motif) ligand 2 (CCL2) production. These data suggest that the phosphocreatine/creatine system links cellular energy shuttling with pro-inflammatory responses in human and murine white adipocytes. Our findings provide unexpected perspectives on the mechanisms driving WAT inflammation in obesity and may present avenues to target adipocyte dysfunction.},
language = {en},
number = {2},
urldate = {2022-02-17},
journal = {Nature Metabolism},
author = {Maqdasy, Salwan and Lecoutre, Simon and Renzi, Gianluca and Frendo-Cumbo, Scott and Rizo-Roca, David and Moritz, Thomas and Juvany, Marta and Hodek, Ondrej and Gao, Hui and Couchet, Morgane and Witting, Michael and Kerr, Alastair and Bergo, Martin O. and Choudhury, Robin P. and Aouadi, Myriam and Zierath, Juleen R. and Krook, Anna and Mejhert, Niklas and Rydén, Mikael},
month = feb,
year = {2022},
keywords = {Fat metabolism, Mechanisms of disease, Obesity},
pages = {1--13},
}
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Herein, we integrate white adipose tissue (WAT) metabolomic and transcriptomic data from clinical cohorts and find that the WAT phosphocreatine/creatine ratio is increased and creatine kinase-B expression and activity is decreased in the obese state. In human in vitro and murine in vivo models, we demonstrate that decreased phosphocreatine metabolism in white adipocytes alters adenosine monophosphate-activated protein kinase activity via effects on adenosine triphosphate/adenosine diphosphate levels, independently of WAT beigeing. This disturbance promotes a pro-inflammatory profile characterized, in part, by increased chemokine (C-C motif) ligand 2 (CCL2) production. These data suggest that the phosphocreatine/creatine system links cellular energy shuttling with pro-inflammatory responses in human and murine white adipocytes. 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