A20 deficiency in myeloid cells protects mice from diet-induced obesity and insulin resistance due to increased fatty acid metabolism
- Author
- Leen Catrysse (UGent) , Bastiaan Maes, Parul Mehrotra (UGent) , Arne Martens (UGent) , Esther Hoste (UGent) , Liesbet Martens (UGent) , Christian Maueröder (UGent) , Anneleen Remmerie, Anna Bujko (UGent) , Karolina Slowicka (UGent) , Mozes Sze (UGent) , Hanna-Kaisa Vikkula (UGent) , Bart Ghesquiere, Charlotte Scott (UGent) , Yvan Saeys (UGent) , Bart van de Sluis, Kodi Ravichandran (UGent) , Sophie Janssens (UGent) and Geert van Loo (UGent)
- Organization
- 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 kappa B (NF-kappa B) 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.
- Keywords
- ADIPOSE-TISSUE, INFLAMMATION, MACROPHAGES, HOMEOSTASIS, HEALTH, LINKS
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Please use this url to cite or link to this publication: http://hdl.handle.net/1854/LU-8727355
- MLA
- 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, no. 12, 2021, doi:10.1016/j.celrep.2021.109748.
- APA
- Catrysse, L., Maes, B., Mehrotra, P., Martens, A., Hoste, E., Martens, L., … 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). https://doi.org/10.1016/j.celrep.2021.109748
- Chicago author-date
- Catrysse, Leen, Bastiaan Maes, Parul Mehrotra, Arne Martens, Esther Hoste, Liesbet Martens, Christian Maueröder, et al. 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). https://doi.org/10.1016/j.celrep.2021.109748.
- Chicago author-date (all authors)
- Catrysse, Leen, Bastiaan Maes, Parul Mehrotra, Arne Martens, Esther Hoste, Liesbet Martens, Christian Maueröder, Anneleen Remmerie, Anna Bujko, Karolina Slowicka, Mozes Sze, Hanna-Kaisa Vikkula, Bart Ghesquiere, Charlotte Scott, Yvan Saeys, Bart van de Sluis, Kodi Ravichandran, Sophie Janssens, and Geert van Loo. 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). doi:10.1016/j.celrep.2021.109748.
- Vancouver
- 1.Catrysse L, Maes B, Mehrotra P, Martens A, Hoste E, Martens L, et al. A20 deficiency in myeloid cells protects mice from diet-induced obesity and insulin resistance due to increased fatty acid metabolism. CELL REPORTS. 2021;36(12).
- IEEE
- [1]L. Catrysse 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, no. 12, 2021.
@article{8727355,
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 kappa B (NF-kappa B) 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.}},
articleno = {{109748}},
author = {{Catrysse, Leen and Maes, Bastiaan and Mehrotra, Parul and Martens, Arne and Hoste, Esther and Martens, Liesbet and Maueröder, Christian and Remmerie, Anneleen and Bujko, Anna and Slowicka, Karolina and Sze, Mozes and Vikkula, Hanna-Kaisa and Ghesquiere, Bart and Scott, Charlotte and Saeys, Yvan and van de Sluis, Bart and Ravichandran, Kodi and Janssens, Sophie and van Loo, Geert}},
issn = {{2211-1247}},
journal = {{CELL REPORTS}},
keywords = {{ADIPOSE-TISSUE,INFLAMMATION,MACROPHAGES,HOMEOSTASIS,HEALTH,LINKS}},
language = {{eng}},
number = {{12}},
pages = {{23}},
title = {{A20 deficiency in myeloid cells protects mice from diet-induced obesity and insulin resistance due to increased fatty acid metabolism}},
url = {{http://doi.org/10.1016/j.celrep.2021.109748}},
volume = {{36}},
year = {{2021}},
}
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