Hepatic expression of genes involved in the core clock machinery and cholesterol metabolism. APOE∗3-Leiden.CETP mice were exposed to 6-h phase advancement every 3 days (circadian disturbance; CD) or regular 12:12 light–dark cycle (Control), while having either ad libitum food access (AL) or food access during the dark phase only (time-restricted feeding; TRF) for a total duration of 14 weeks. Hepatic gene expression of (A) brain and muscle Arnt-like protein-1 (Bmal1), (B) period 2 (Per2), (C) circadian locomotor output cycles kaput (Clock), (D) microsomal triglyceride transfer protein (Mttp), (E) apolipoprotein B (Apob), (F) cholesterol 7 alpha-hydroxylase (Cyp7a1), (G) ATP-binding cassette sub-family G member 5 (Abcg5), (H) sterol regulatory element-binding protein 2 (Srebp2), and (I) 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (Hmgcr) at Zeitgeber time (ZT) 0 and 12, as determined by quantitative polymerase chain reaction, normalized to glyceraldehyde-3-phosphate dehydrogenase (Gapdh) and shown relative to the expression in control AL ZT0 (n = 5–8 mice/group/time point). Data are presented as means ± SD. $CD + AL vs. CD + TRF; ∗ Control + AL vs. CD + AL; &Control + TRF vs. CD + TRF. ∗P < 0.05; $$ P < 0.01; ∗∗∗,&&& P < 0.001, according to two-way ANOVA and following Tukey's multiple-comparison test.