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. Author manuscript; available in PMC: 2018 Mar 13.
Published in final edited form as: Obesity (Silver Spring). 2016 Nov 2;25(1):155–165. doi: 10.1002/oby.21701

Figure 3. OCA failed to activate hepatic FXR.

Figure 3

Whole liver lysate cytosolic and nuclear protein expression levels for (A) farnesoid X receptor (FXR) and (B) sterol regulatory element-binding protein 1 (SREBP1) in atherogenic diet-fed foz/foz mice vs. Wt, with or without OCA treatment. In addition, we compared mRNA expression levels of (C) small heterodimer partner (Shp), liver X receptor-alpha (Lxr-α), and cholesterol 7α-hydroxylase (Cyp7a1), as well as (D) PPAR-γ co-activator 1-alpha (Pgc1-α) and (E) ATP-binding cassette subfamily A member 1 (Abca1), Srebp1, acyl-coenzyme A dehydrogenase, long chain (Acadl), peroxisomal acyl-coenzyme A oxidase 1 (Acox1), and cytochromes P450 4A10 (Cyp4a10) and 4A14 (Cyp4a14), for which their expression may be regulated by OCA, and that are relevant to the intracellular lipid metabolism in liver. Data are mean ± SEM (n=9-10/gp). *P<0.05 vs. genotype-matched control (treatment effect), δP<0.05 vs. treatment-matched control (genotype effect).