The infiltration of macrophages is a primary event in obesity-induced adipose tissue inflammation.36–38 In obesity, adipocytes produce CCL2 and S100A8, which recruit CCR2-expressing pro-inflammatory M1 macrophages and monocytes to adipose tissue.36–38,40 We found that αKetoA did not alter the expression levels of Ccl2 and S100a8; instead, αKetoA—in a PPARγ-dependent manner—prevented macrophages from infiltrating the adipose tissues of obese mice and inhibited fibrosis and the formation of crown-like structures. Here, CCL2 is linked to obesity due to melanocortin 4 receptor deficiency.