Fig. 2.
Impairment of PPARα activity augments hepatic VLDL biogenesis. A and B: PPARα+/+ and PPARα−/− mice were fasted for 5 h, and blood collection was performed every hour after ip injection of poloxamer. Triglyceride (TG) and cholesterol (CHOL) levels were assessed at 0, 1, 2 and 3 h (A), and VLDL TG was assessed at 3 h (B). C: McA cells (1 × 106) were untreated or treated with MK-866 (10 μM) for 48 h, deprived of methionine and cysteine for 1 h in the presence or absence of MK-866 (10 μM), and then pulsed with 100 μCi/ml [35S]methionine in the presence of oleate (400 μM) for 3 h. Media were collected and subjected to fractionation by ultracentrifugation, fractions were collected, and 35S-labeled apolipoprotein B (apoB)-100 and 35S-labeled apolipoprotein E (apoE) were immunoprecipitated with anti-apoB and anti-apoE antibodies, respectively. For animal studies, results are shown as means ± SE (n = 5–6/group). For in vitro studies, data represent 3 experiments. *P < 0.05 vs. controls.