Fig. 4

Loss of AKR1A1 aggravates alcohol-induced liver steatosis. The mRNA levels of the related marker genes involved in fatty acid (FA) transport and activation (Cd36, Vldlr, Fatp1, and Lpl) (A), FA oxidation (Cpt1α, Acox1, and Pparα) (B), and FA synthesis (Acaca, Fasn, Srebp1, and Lipin1) (C) were examined by qRT‒PCR to evaluate the effects of AKR1A1 loss on alcohol-induced liver steatosis. Values were normalized to the β-actin gene and expressed in relation to the PF-treated WT mice. The frozen liver sections were subjected to Oil Red O (ORO) staining (E), and the relative fat accumulation was compared by the quantification of ORO-positive stained areas (D). Western blot analysis of ADRP, SREBP1, FASN, and pACC/ACC expression in the liver is shown in Panel (F), in which the relative protein levels were quantified by β-actin normalization. Data are presented as the means ± SD (n ≥ 3). Statistical differences are marked as follows: ^#p < 0.05, ^##p < 0.01, ^###p < 0.001 (compared with the PF-treated WT group); *p < 0.05, **p < 0.01, ***p < 0.001 (compared between the other groups)