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Mechanistically, we show that GPR120 is a PPARγ target gene in adipocytes, while GPR120 augments PPARγ task by causing the endogenous ligand 15d-PGJ2 and by preventing ERK-mediated inhibition of PPARγ. Further, we used macrophage- (MKO) or adipocyte-specific GPR120 KO (AKO) mice to show that GRP120 has anti inflammatory impacts via macrophages while working with PPARγ in adipocytes to improve insulin susceptibility. These results improve the prospect of a safer option to boost i
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