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. 2004 Jan 15;18(2):157–169. doi: 10.1101/gad.1138104

Figure 6.

Figure 6.

PGC-1α and FXR regulate triglyceride synthesis and secretion. (A) Ectopic expression of PGC-1α decreases triglyceride synthesis in primary hepatocytes. Wild-type and FXR-null primary hepatocytes were infected with adenovirus expressing GFP or PGC-1α. After 48 h, 14C-palmitic acid was added to the media. After an additional 2 h, the media and hepatocytes were separated and the radioactive triglyceride levels were determined, as described in Materials and Methods. Values are the means ± SE (n = 3). (B) Ectopic expression of PGC-1α decreases triglyceride secretion in an FXR-dependent manner. FXR+/+ or FXR-/- primary hepatocytes were infected with Ad-GFP or Ad-PGC-1α for 48 h and then incubated with 14C-palmitic acid for 2 h, as described in A. The radioactive triglyceride in the media was determined and the values were shown, mean ± SE (n = 3). (C,D) Ectopic expression of PGC-1α decreases SREBP-1c and FAS expression. Primary hepatocytes were infected with Ad-GFP or Ad-PGC-1α for 48 h. Real-time PCR was used to analyze the relative expression of SREBP-1c and fatty acid synthase (FAS). (E,F) Activation of FXR decreases SREBP-1c expression. Primary hepatocytes were treated with FXR ligand GW4064 (1 μM) or CDCA (100 μM) for 24 h. Real-time PCR was used to analyze the relative expression of SREBP-1c and SHP expression. (*) p < 0.05; (**) p < 0.01.