期刊
CELL REPORTS
卷 36, 期 12, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.celrep.2021.109748
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资金
- Instituut voor Innovatie door Wetenschap en Technologie'' (IWT)
- Kom op tegen Kanker
- German Research Foundation (DFG) [MA 7770/1-1]
- FWO
- Belgian Foundation against Cancer
- Geneeskundige Stichting Koningin Elisabeth'' (GSKE)
- Interuniversity Attraction Poles program'' (IAP7)
- Concerted Research Actions'' (GOA) of the Ghent University
The study found that myeloid-specific A20-deficient mice are protected from diet-induced obesity and insulin resistance despite the presence of an inflammatory environment in their metabolic tissues. Macrophages lacking A20 show impaired mitochondrial respiratory function and metabolize more palmitate, resulting in a lean phenotype and protection from metabolic disease. These findings suggest a role for A20 in regulating macrophage immunometabolism.
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.
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