FIGURE 3.

PPARδ increases glucose utilization in primary hepatocytes. A–C, PPARδ increases glucose flux to glycogen synthesis, lipogenesis, and glycolysis determined by radioactive tracers. Hepatocytes infected with GFP or PPARδ virus were labeled with [¹⁴C]glucose without or with 100 nm insulin. The conversion of radioactive glucose to glycogen, fatty acid, and CO₂ (to estimate glycolysis) was determined and normalized to protein content. D, fatty acid β-oxidation assay determined by [³H]palmitate. E, the expression of glucokinase (GK), GLUT2, and lipogenic genes is up-regulated in hepatocytes infected with adenoviral PPARδ. Gene expression was determined by real time qPCR 48 h post-infection. F, assessment of target gene regulation by endogenous PPARδ. Primary hepatocytes from wild type (wt) and liver-specific PPARδ^−/− (ko) mice were given 0.1 μm GW501516 for 6 h, and gene expression was examined by real time qPCR. *, p < 0.05.