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 3
Adequate response to glucose occurs in the absence of LXR. (A) qRT-PCR analysis of GK, ChREBP, L-PK, ACC, SREBP-1c, FAS, SCD1, GPAT, LXRα, LXRβ, ABCG1, and ABCA1 in livers from wild-type and LXRα/β knockout mice either fasted overnight or challenged with a HCHO diet for 18 h. Error bars represent SD. n = 5–8 per group. (B) Blood glucose concentrations and liver G6P and glycogen content in wild-type and LXRα/β knockout mice either fasted or HCHO refed. *P < 0.05, **P < 0.001 versus fasted. n.d., not detectable. (C) Cytosolic and nuclear ChREBP protein in liver extracts from fasted and HCHO-refed wild-type and LXRα/β knockout mice. Lamin A/C and β-actin antibodies were used as loading controls. A representative Western blot is shown (n = 5–8 per group). Lanes were run on the same gel but were noncontiguous. (D) Precursor and mature SREBP-1 protein in liver lysates from fasted and HCHO-refed wild-type and LXRα/β knockout mice. β-Actin was used as a loading control. A representative Western blot is shown (n = 5–8 per group). Lanes were run on the same gel but were noncontiguous.