ChREBP, but not LXRs, is required for the induction of glucose-regulated genes in mouse liver
J. Clin. Invest. Pierre-Damien Denechaud, et al. 118:956 doi:10.1172/JCI34314 [Go to this article.]

Figure 2
Differential regulation of ChREBP by LXRs and glucose. (A) Quantitative real-time RT-PCR (qRT-PCR) analysis of GK, ChREBP, L-PK, ACC, SREBP-1c, FAS, SCD1, LXRα, and ABCG1 in livers of C57BL/6J mice treated for 3 days with either vehicle or 50 mg/kg body weight of the synthetic LXR agonist T0-901317. After treatment, mice were fasted overnight or maintained in the fed state. Results are mean ± SEM (n = 6 per group). ^#P < 0.005 vs. fasted; *P < 0.05, **P < 0.001 vs. vehicle. (B) Total, cytosolic, and nuclear ChREBP protein in liver extracts from vehicle- and T0-901317–treated fasted and fed mice. Lamin A/C and β-actin antibodies were used as loading controls. A representative Western blot is shown (n = 6 per group). (C) Ser196 phosphorylation level of the endogenous ChREBP protein. A representative Western blot is shown (n = 6 per group). Quantification of the ratio of Ser196 ChREBP phosphorylation to total ChREBP protein content is shown. *P < 0.05 vs. fasted T0-901317–treated. ChREBP immunofluorescence analysis in liver sections from T0-901317–treated fasted and vehicle-treated fed mice. Original magnification, ×400. n = 6 per group. (D) qRT-PCR analysis of ChREBP and L-PK in mouse hepatocytes incubated in the presence of low glucose (5 mM; G5) plus DMSO (white bars) or 10 μM T0-901317 (black bars) or in the presence of high glucose concentrations (25 mM) plus 100 nM insulin (gray bars) for 24 h. Error bars represent SD (n = 4 independent cultures). *P < 0.005 vs. 5 mM glucose plus DMSO.