Animals were treated with CoCl₂ as described in Figure 9 and used to collect tissues (n = 6 per group), to study hepatic [³H]OA uptake or [¹⁴C]OA oxidation (n = 6 per group), or for isolation of Kupffer cells (n = 6 per group). (A and B) Triglyceride levels decreased (A) but TBARS increased (B) in livers of CoCl₂-injected Clk^Δ19/Δ19 Apoe^−/− mice. (C) Plasma ALT levels increased in CoCl₂-injected Clk^Δ19/Δ19 Apoe^−/− mice. In contrast, plasma β-HB concentrations decreased in CoCl₂-injected Clk^Δ19/Δ19 Apoe^−/− mice. (D) Livers from CoCl₂-injected Clk^Δ19/Δ19 Apoe^−/− mice assimilated less [³H]OA than controls. (E) Liver slices from CoCl₂-injected Clk^Δ19/Δ19 Apoe^−/− mice were used to study fatty acid uptake and oxidation. (F) Expression of lipoprotein assembly and β-oxidation genes was reduced in CoCl₂-injected Clk^Δ19/Δ19 Apoe^−/− mice. Mean ± SD; *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, multiple t tests. (G) Kupffer cells isolated from CoCl₂-injected Clk^Δ19/Δ19 Apoe^−/− mice took up more DiI-labeled AcLDL (5 μg/mL). Kupffer cells were incubated with DiI-labeled AcLDL (5 μg/mL) for 4 hours. Cells were washed, lipids were extracted, and dye was measured at 485 nm. (H) Kupffer cells isolated from CoCl₂-injected Clk^wt/wt Apoe^−/− and Clk^Δ19/Δ19 Apoe^−/− mice were incubated with DiI-AcLDL. Mean ± SD; ***P < 0.001, 2-way ANOVA, Šidák’s multiple-comparisons test. (I) mRNA levels of different genes in isolated Kupffer cells from CoCl₂-injected mice. Mean ± SD; ***P < 0.001, ****P < 0.0001, multiple t tests. (J) ChIP assays were performed in Kupffer cells isolated from livers of indicated mice to study the binding of HIF1α to the Cd36 promoter. Data are representative of 2 experiments.