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. 2019 May 6;25:83–94. doi: 10.1016/j.molmet.2019.05.002

Figure 2.

Figure 2

Loss of ABHD15 resulted in impaired insulin regulation of lipolysis with no defect in glucose uptake. Lipolysis (A-C) and glucose uptake (D-F) was assessed either in 3T3-L1 adipocytes infected with shRNA against ABHD15 (shABHD) or control (shCtrl, A, D), or in wild type (WT) and ABHD15−/− (KO) brown adipocytes (B, E), or in visWAT explants from wild type and ABHD15−/− mice (C, F). ABHD15 was re-expressed (+WT) in knockdown (A, D) or knockout adipocytes (B, E) with control cells infected with empty vector (+EV). Glycerol release (A-C) or [3H]-2-deoxyglucose ([3H]-2DG) uptake (D-F) was assessed in adipocytes or fat explants in response to indicated treatments (CL, CL316,243). Data are mean ± SEM with individual data points shown (n = 3–5, except D: KD + WT (n = 2, mean ± SD)); * different from without insulin, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; § different from without CL, §p < 0.05, §§p < 0.01, §§§§p < 0.0001; # different from KD/KO, #p < 0.05, ##p < 0.01, ###p < 0.001, ####p < 0.0001; statistical significance was determined using two-way ANOVA with Tukey's multiple comparison test.