Figure 3
ESR1 inhibition of gluconeogenic gene expression is E2 dependent. (A,B) Hepatic mRNA levels of G6Pase and Pck1 from Control mice and LERKO mice (n >= 6 per genotype). (C,D) Primary hepatocytes from Control mice were treated with vehicle or different doses of E2 (10−12 M, 10−11 M, 10−10 M, 10−9 M, 10−8 M), mRNA levels of G6Pase and Pck1 were measured by q-RT-PCR. F-H, primary hepatocytes from Control and LERKO mice were treated with vehicle or different doses of E2 (10−10 M, 10−9 M, 10−8 M), mRNA levels of G6Pase and Pck1 were measured by q-RT-PCR. (E,F) Primary hepatocytes from Control and LERKO mice were treated with vehicle or different doses of E2 (10−10 M, 10−9 M, 10−8 M), mRNA levels of G6Pase and Pck1 were measured by q-RT-PCR.G-H, ChIP assay experiments were performed with liver tissues using antibody to ESR1, or with rabbit preimmune serum (IgG) and primers flanking the G6Pase (G) and Pck1 (H) promoters. Real-time PCR data with an inset of a 1.5% agarose gel as a representative example. Results were normalized to input and shown as fold enrichment IgG from 3 independent ChIP experiments. The experiments were performed 2 weeks after virus injection. The data are expressed as the means ± SD, *p < 0.05 versus control, *p < 0.05 versus vehicle, ### p < 0.001 versus control.
