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. Author manuscript; available in PMC: 2019 Sep 13.
Published in final edited form as: Hepatology. 2018 May 20;68(3):883–896. doi: 10.1002/hep.29878

FIG. 4.

FIG. 4.

Hepatic Bmal1 deficiency results in decreased gene expression of both de novo lipogenesis and β-oxidation in the liver of ethanol-fed mice. (A-C) Hepatocyte-specific deficiency of Bmal1 results in decreased PPARα activity in BLKO mice liver after ethanol treatment. Mice were treated as described in Fig. 1. Relative mRNA levels of lipogenic genes (A) and PPARα target genes (B), and protein levels of PPARα (C) in the livers of Bmal1-LKO mice (n=5), were compared to those of Bmal1Flox/Flox mice (n=4). (D-F) Adult-onset Bmal1 depletion in the liver decreases the PPARα activity after ethanol treatment. Relative mRNA levels of lipogenic genes (D) and PPARα target genes (E), and protein levels of PPARα (F) in the livers of Ad-shBmal1-injected mice (n=8), were compared with those of Ad-shLacZ control (n=5). *p < 0.05, ***p < 0.001 by two-tailed Student’s t test.