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. 2020 Oct 31;43:101108. doi: 10.1016/j.molmet.2020.101108

Figure 1.

Figure 1

The loss of hepatic ChREBP prevents non-alcoholic fatty liver disease in L.G6pc−/−mice. Control and L.Chrebp−/− mice (pink bars) and L.G6pc−/− and L.G6pc−/−.Chrebp−/− mice (red bars) were fed a standard during 10 days after tamoxifen treatment. (A) Hepatic TG and cholesterol content (n = 6–8/group); (B, D and E) Relative mRNA expression of genes involved in lipid metabolism and lipid transport (n = 5–6/group). (C) Relative expression of FAS, CD36 and phosphorylated (P-ACC) or total ACC protein analysed by western blot. Representative images of blots (n = 3) and quantification graphs (6–8 samples/group) are shown. The quantification of FAS and CD36 was performed relatively to total amount of proteins using stained-free imaging technology (See Figure S5). The quantification of P-ACC was expressed relatively to the total ACC protein quantity. Data are expressed as mean ± s.e.m. ∗p < 0.05, ∗∗p < 0.01 and ∗∗∗p < 0.001 indicate significance compared to control mice; $p < 0.05, $$p < 0.01 and $$$p < 0.001 indicate significance compared to L.G6pc−/− mice; £p < 0.05, ££p < 0.01 and £££p < 0.001 indicates significance compared to L.Chrebp−/− mice. See also Figure S2.