SUCNR1 controls an anti-inflammatory program in macrophages to regulate the metabolic response to obesity

Identifier:  TFG:5002

Handle: https://hdl.handle.net/20.500.11797/TFG5002

Authors:  Keiran Fernández, Noelia Elizabeth

Abstract:
Succinate is a signaling metabolite sensed extracellularly by SUNCR1 receptor. The accumulation of succinate in macrophages is known to activate a pro-inflammatory program; however, the contribution of SUCNR1 to macrophage phenotype and function has remained unclear. We found that activation of SUCNR1 had a critical role in the anti-inflammatory responses in macrophages. Myeloid-specific deficiency in SUCNR1 promoted a local pro-inflammatory phenotype, disrupted glucose homeostasis in mice fed a normal chow diet, exacerbated the metabolic consequences of diet-induced obesity and impaired adipose-tissue browning in response to cold exposure. Activation of SUCNR1 promoted an anti-inflammatory phenotype in macrophages and boosted the response of these cells to type 2 cytokines