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. 2019 May 2;60(7):1284–1292. doi: 10.1194/jlr.M093369

Fig. 4.

Fig. 4.

MGL inhibition promotes lipid storage in 3T3-L1 cells and APCs via PPARγ regulation. A: Mgl and Pparγ gene expression during 3T3-L1 differentiation time course (13 days). B: mRNA gene expression of Pparγ2, adiponectin, and leptin after JZL184 treatment resulted in augmented expression of lipogenic genes. C: BODIPY flow cytometry staining of nontreated (Ctrl) and JZL184-treated 3T3-L1 cells with representative dot plots demonstrates increased lipid content. mRNA gene expression analysis of adipogenic genes Dgat1, Pparγ2, and adiponectin in APCs isolated from WT animals (D) and APCs from MGL−/− mice upregulated (E). F: Protein expression of PPARγ and β-actin with densitometric analysis. G: mRNA gene expression of Mgl, Pparγ2, and Cd36 of 3T3-L1 cells treated with rosi or pio for 48 h significantly increased. H: MGL mRNA relative (rel.) expression of fully differentiated 3T3L1 treated with GW9662 alone (a potent antagonist of PPARγ) or in combination with rosi. Mean of three independent experiments ± SD value. * P ≤ 0.05, treatment versus control; # rosiglitazone versus control.