Figure 4.

PPARα Mediates the Regulation of sKL on Hepatic Glucose and Lipid Metabolism in T2D

WT DM, KL^+/− DM, and TgKL DM were fed with a HFD for 8 weeks (n = 8/group). (A) The protein levels of PPARα in the livers of the three groups were subjected to western blot analysis. (B) IF staining of PPARα (green) in liver sections from the three groups. Nuclei were labeled in blue using 4′,6-diamidino-2-phenylindole (DAPI). (C) Hepatic glucose production (HGP) in mouse primary hepatocytes derived from TgKL DM treated with glucagon applied with GW6471 or not. (D) 2-DG uptake levels of cells with GW6471 or not were tested. (E) Oil red O staining of cells with GW6471 or not were performed. (F) Cellular supernatant levels of inflammatory factors (TNF-α and IL-1β) in cells were determined. (G–I) Protein levels of GCK and PEPCK (G) and mRNA levels of GCK (H) and PEPCK (I) in cells with GW6471 or not. Scale bars, 50 μm. For all statistical plots, the data are presented as the mean ± SD; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.