In obesity-associated inflammation, adipocytes produce CCL2 and S100A8 for the recruitment of macrophages.36–38,40 Treatment with αKetoA had little effect on the expression of Ccl2 and S100a8 in adipocytes (Supplementary Fig. S6), suggesting that αKetoA acted directly on macrophages to inhibit their infiltration into adipose tissues and to alter macrophage polarization to M2 phenotypes. This evidence concerns the gene S100A8 and obesity disorder.