Fig. 1.

LXRs confer differential regulation of hepatic ChREBP isoform expression. C57BL/6 control and STZ-treated male mice were fasted (white bars) or fasted-refed for 12 h (black bars). A: Insulin and glucose levels. B: Hepatic gene expression of Lxrα/β, Srebp-1, Mlx, and Chrebpα/β was analyzed by quantitative RT-PCR and normalized to Tbp. C: Nuclear lysates were subjected to SDS-PAGE and immunoblotted with antibodies against LXR, SREBP-1, and ChREBP. Cytosolic levels of SREBP-1 and ChREBP are also shown. α-Tubulin and lamin A were used as controls for cytosolic and nuclear fractions, respectively. Each lane represents independent mice from experimental groups. The samples for control and STZ-treated mice were loaded on separate gels and the films were developed with the same exposure time. One representative Western blot is shown (n = 2). D: LXR binding to LXRE-containing promoter regions of SREBP-1c and ChREBP were analyzed by ChIP with antibody recognizing LXRα/β. All values are mean ± SEM (n = 4–5). *P < 0.05, **P < 0.01, ***P < 0.001 compared with fasted within experimental groups. ^#P < 0.05, ^##P < 0.01, ^###P < 0.001 compared with refed within STZ treatment.