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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. 4. AMPK suppresses the cleavage processing and nuclear translocation of SREBP-1 in human HepG2 cells or in diabetic mouse livers.

Fig. 4

A. and B. Overexpression of DN-AMPK abolishes the inhibitory effect of resveratrol on accumulation of nuclear SREBP-1 in HepG2 cells exposed to high glucose or high glucose plus insulin. C. DN-AMPK abrogates the effect of S17834 to reduce the nuclear SREBP-1 in isolated hepatocytes. After a 24-h period of infection with Ad-GFP or Ad-DN-AMPK, HepG2 cells or primary hepatocytes were incubated in serum free DMEM containing 5.5 mM overnight and treated for an additional 24 h with resveratrol or S17834 in the presence of high glucose (30 mM) or high glucose (30 mM) and insulin (100 nM). D. Enhanced nuclear translocation of SREBP-1 in response to high glucose or high glucose plus insulin is prevented by either S17834 or metformin in HepG2 cells. Immunoblot analysis of SREBP-1 in cytoplasmic and nuclear extracts is shown. E. Confocal of immunofluorescent images show SREBP-1 staining (Green) and nuclear staining with propidium iodide (PI, Red) in HepG2 cells. F. S17834 and metformin decrease lipid accumulation in HepG2 cells exposed to high glucose (HG) plus insulin, as reflected by Oil Red O staining. G. Increased nuclear translocation of SREBP-1 is increased in the hepatocytes of insulin resistant mice and eliminated by S17834. A representative confocal microscopy image of immunofluorescent staining of liver sections for SREBP-1 (Green) and nuclear (Red) is shown. Arrows represent SREBP-1 localization in nucleus of hepatocytes, original magnification, 60.