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Catrysse L, Maes B, Mehrotra P, et al. A20 deficiency in myeloid cells protects mice from diet-induced obesity and insulin resistance due to increased fatty acid metabolism. Cell Rep. 2021;36(12):109748doi: 10.1016/j.celrep.2021.109748.
Catrysse, L., Maes, B., Mehrotra, P., Martens, A., Hoste, E., Martens, L., Maueröder, C., Remmerie, A., Bujko, A., Slowicka, K., Sze, M., Vikkula, H., Ghesquière, B., Scott, C. L., Saeys, Y., van de Sluis, B., Ravichandran, K., Janssens, S., & van Loo, G. (2021). A20 deficiency in myeloid cells protects mice from diet-induced obesity and insulin resistance due to increased fatty acid metabolism. Cell reports, 36(12), 109748. https://doi.org/10.1016/j.celrep.2021.109748
Catrysse, Leen, et al. "A20 deficiency in myeloid cells protects mice from diet-induced obesity and insulin resistance due to increased fatty acid metabolism." Cell reports vol. 36,12 (2021): 109748. doi: https://doi.org/10.1016/j.celrep.2021.109748
Catrysse L, Maes B, Mehrotra P, Martens A, Hoste E, Martens L, Maueröder C, Remmerie A, Bujko A, Slowicka K, Sze M, Vikkula H, Ghesquière B, Scott CL, Saeys Y, van de Sluis B, Ravichandran K, Janssens S, van Loo G. A20 deficiency in myeloid cells protects mice from diet-induced obesity and insulin resistance due to increased fatty acid metabolism. Cell Rep. 2021 Sep 21;36(12):109748. doi: 10.1016/j.celrep.2021.109748. PMID: 34551300.
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Cell Rep. 2021 Sep 21;36(12):109748. doi: 10.1016/j.celrep.2021.109748.

A20 deficiency in myeloid cells protects mice from diet-induced obesity and insulin resistance due to increased fatty acid metabolism.

Cell reports

Leen Catrysse, Bastiaan Maes, Parul Mehrotra, Arne Martens, Esther Hoste, Liesbet Martens, Christian Maueröder, Anneleen Remmerie, Anna Bujko, Karolina Slowicka, Mozes Sze, Hanna Vikkula, Bart Ghesquière, Charlotte L Scott, Yvan Saeys, Bart van de Sluis, Kodi Ravichandran, Sophie Janssens, Geert van Loo

Affiliations

  1. VIB Center for Inflammation Research, B-9052 Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, 9052 Ghent, Belgium.
  2. VIB Center for Inflammation Research, B-9052 Ghent, Belgium; Department of Internal Medicine and Pediatrics, Ghent University, B-9052 Ghent, Belgium.
  3. Metabolomics Core Facility, VIB Center for Cancer Biology, VIB, B-3000 Leuven, Belgium.
  4. VIB Center for Inflammation Research, B-9052 Ghent, Belgium; Department of Applied Mathematics, Computer Science and Statistics, Ghent University, B-9052 Ghent, Belgium.
  5. Department of Pediatrics, Molecular Genetics Section, University of Groningen, University Medical Center Groningen, NL- 9713 Groningen, the Netherlands.
  6. VIB Center for Inflammation Research, B-9052 Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, 9052 Ghent, Belgium; Center for Cell Clearance and Department of Microbiology, Immunology and Cancer Biology, University of Virginia, Charlottesville, VA, USA.
  7. VIB Center for Inflammation Research, B-9052 Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, 9052 Ghent, Belgium. Electronic address: [email protected].

PMID: 34551300 DOI: 10.1016/j.celrep.2021.109748

Abstract

Obesity-induced inflammation is a major driving force in the development of insulin resistance, type 2 diabetes (T2D), and related metabolic disorders. During obesity, macrophages accumulate in the visceral adipose tissue, creating a low-grade inflammatory environment. Nuclear factor κB (NF-κB) signaling is a central coordinator of inflammatory responses and is tightly regulated by the anti-inflammatory protein A20. Here, we find that myeloid-specific A20-deficient mice are protected from diet-induced obesity and insulin resistance despite an inflammatory environment in their metabolic tissues. Macrophages lacking A20 show impaired mitochondrial respiratory function and metabolize more palmitate both in vitro and in vivo. We hypothesize that A20-deficient macrophages rely more on palmitate oxidation and metabolize the fat present in the diet, resulting in a lean phenotype and protection from metabolic disease. These findings reveal a role for A20 in regulating macrophage immunometabolism.

Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.

Conflict of interest statement

Declaration of interests The authors declare no competing interests.

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