Fig. 2. Para-chlorophenylalanine (PCPA) treatment suppressed the positive hepatic lipid balance. Eight-week-old mice were fed a standard chow diet (SCD) or high fat diet (HFD) for 12 weeks and treated with vehicle or PCPA treatment. Hepatic expressional profiles of genes related to de novo lipogenesis (A), triglyceride synthesis (B), fatty acid (FA) uptake (C), FA oxidation (D), very low density lipoprotein secretion (E), and transcription factors (F) were assessed by quantitative reverse transcription polymerase chain reaction (n=6). Acaca, acetyl-CoA carboxylase alpha; Fasn, fatty acid synthase; Acly, ATP citrate lyase; Me1, malic enzyme 1; Scd1, stearoyl-CoA desaturase 1; Gpam, glycerol-3-phosphate acyltransferase; Agpat1, 1-acylglycerol-3-phosphate O-acyltransferase 1; Lpin1, lipin 1; Mogat1, monoacylglycerol O-acyltransferase 1; Dgat1, diacylglycerol O-acyltransferase 1; Dgat2, diacylglycerol O-acyltransferase 2; Cpt1a, carnitine palmitoyltransferase 1a; Mttp, microsomal triglyceride transfer protein; Apob, apolipoprotein B; Pparg, peroxisome proliferator activated receptor gamma; Ppargc1a, Pparg coactivator 1 alpha; Srebp1c, sterol regulatory element binding transcription factor 1c; Mlxipl, MLX interacting protein-like (ChREBP, carbohydrate response element binding protein); Nr1h3, nuclear receptor subfamily 1, group H, member 3 (LXR, liver X receptor). ^aP<0.05, ^bP<0.01, ^cP<0.001.