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. 2019 May 28;20(11):2625. doi: 10.3390/ijms20112625

Figure 1.

Figure 1

Decrease in lipogenesis enzymes after docosahexaenoic acid (DHA) treatment. (A,B) The protein expression level of fatty acid synthase (FAS), acetyl-coenzyme A carboxylase (ACC), stearoyl-CoA desaturase-1 (SCD-1) and precursor form of SREBP-1 (preSREBP-1). Mouse primary hepatocytes were treated with DHA 300 μM or eicosapentaenoic acid (EPA) 300 μM for 12 h. Data represent means ± SD (n = 5). GAPDH: Glyceraldehyde 3-phosphate dehydrogenase. (C) In order to screen an optimal DHA concentration that exerts potent antilipogenic effects, primary hepatocytes were treated with DHA 100 μM and 300 μM for 12 h followed by T0901317 (T090), liver X receptor (LXR) agonist for additional 12 h. Data represent means ± SD (n = 5), *** p < 0.005 compared with the control group; ### p < 0.005 compared with the T090-treated group (D) Effects of DHA on the expression of lipogenic proteins stimulated by LXR agonist. Primary hepatocytes were treated with DHA 300 μM for 12 h followed by T090 for additional 12 h. Data represent means ± SD (n = 5), *** p < 0.005 compared with the control group; ### p < 0.005 compared with the T090-treated group (E) Effects of DHA on the expression of lipogenic proteins in high glucose with insulin condition. Primary hepatocytes were treated with DHA 300 μM for 12 h followed by 30 mM high-glucose medium for 30 min and further incubation with 200 nM insulin for 24 h. Data represent means ± SD (n = 3), *** p < 0.005 compared with the control group; ### p < 0.005 compared with the high glucose and insulin group.