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. Author manuscript; available in PMC: 2012 Apr 6.
Published in final edited form as: Cell Metab. 2011 Apr 6;13(4):376–388. doi: 10.1016/j.cmet.2011.03.009

Fig. 5. AMPK represses the transcriptional activity of SREBP-1c and its lipogenic target gene.

Fig. 5

A. CA-AMPK is sufficient to suppress enhanced SREBP-1-dependent de novo lipogenic gene expression in HepG2 cells exposed to high glucose. The mRNAs encoding SREBP-1a, −1c and FAS were analyzed by real-time RT-PCR. B. AMPK is required for polyphenols to reduce mRNA levels of SREBP-1c and FAS in HepG2 cells exposed to high glucose. Data are presented as the mean ± S.E.M., n=3–4, *P<0.05, vs normal glucose; #P<0.05, vs high glucose. C. SRE motif is responsible for AMPK to repress transcriptional activity on SREBP-1c promoter. The proximal promoter regulatory region of human SREBP-1c contains its cis-acting elements: two SRE elements and the putative NF-Y and SP-1 sites. HepG2 cells were cotransfected with empty plasmid pGL3, luciferase reporter plasmids containing wild type human SREBP-1c promoters (−1470/+90 and −257/+90), or the mutant reporter with disrupted SRE, together with Renilla luciferase reporter plasmid pRL-SV40. Thirty two hours post transfection, cells were cultured in serum-free DMEM and treated with or without polyphenols for 16 h. D. DN-AMPK enhances the transcription activity of SREBP-1c promoter (−1470/+90) and abrogates the inhibitory effect of resveratrol in HepG2 cells. E. AMPK−/− MEFs exhibit enhanced FAS promoter activity. *P<0.05, vs AMPK+/+MEFs. F. Suppression of FAS gene transcription in response to AICAR and S17834 is diminished by DN-SREBP-1c. G. AMPK suppresses FAS promoter activity in a SREBP-1c dependent manner. *P<0.05, vs untreated group. *P<0.05, vs treatment group.