Figure 6.

A, The human ChREBP promoter (−2092/+32 bp) coupled to the luciferase reporter construct (pGL4) was cotransfected into CV-1 cells in the presence of an expression vector for TR-β1 and/or RXR-α (0.5 μg/well in a six well format) as indicated in the figure. Vector, pSG5. Relative luciferase activities (for both ± T₃ groups) (mean ± se, n = 3) compared with the light units of the reporter construct in the absence of T₃ (10⁻⁸ m) (arbitrary light units divided by cellular protein) are shown as relative expression (fold). *, P < 0.01 by t testing. B, The contribution of T₃ to the hepatic lipid metabolism. Schematic diagram illustrates the relationship between T₃ and key factors in hepatic lipid metabolism. T₃ induces LXR-α gene expression and represses SREBP-1c mRNA levels, which promotes ACC and malicenzyme (ME) upon insulin signaling. Insulin represses LXR-α gene expression. LXR-α positively regulates both ChREBP and SREBP-1c gene expression and stimulates fatty acid synthase. T₃ induces ChREBP gene expression and ChREBP promotes L-PK and ME by glucose.