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

Figure 4.

Figure 4

Role of GPR40 in expression of lipogenesis enzymes in hepatocytes. (A) Primary hepatocytes were treated with AMG-1638 (1 and 3 μM) for 12 h followed by T090 for additional 12 h, and total cell lysates were subjected to immunoblotting for preSREBP-1 and SCD-1. Data represent means ± SD (n = 4), ***P < 0.005 compared with the control group; # p < 0.05, ### p <0.005 compared with the T090-treated group. (B) Inhibitory effects of AMG-1638 on the protein expression of lipogenic enzymes in high glucose and insulin condition. Primary hepatocytes were treated with 3 μM AMG-1638 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 = 4), *** p < 0.005 compared with the control group, ### p < 0.005 compared with the T090-treated group. (C) Primary hepatocytes were treated with DHA and 10 μM GW1100, GPR40 antagonist 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 = 4), *** p < 0.005 compared with the control group; # p < 0.05, ### p < 0.005 compared with the T090-treated group; + p < 0.05, +++ p < 0.005 compared with the T090 and DHA treated group. (D) In GPR120 KO hepatocytes, 10 μM GW1100 reversed the antilipogenic effects of DHA. Data represent means ± SD (n = 4). *** p < 0.005 compared with the control group; # p < 0.05, ### p < 0.005 compared with the T090-treated group; +p < 0.05, +++ p < 0.005 compared with the T090 and DHA treated group.