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. 2011 Jun 23;301(4):G739–G747. doi: 10.1152/ajpgi.00432.2010

Fig. 1.

Fig. 1.

A: treatment of H4IIEC3 cells with AMP-activated protein kinase (AMPK) activators results in increased phosphorylation of AMPK. H4IIEC3 cells were treated with metformin or 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) for 24 h before harvesting and Western blotting for phospho-AMPK. Bars between columns signify noncontiguous lanes on the same gel. B: H4IIEC3 cells were transfected with a proliferator-activated receptor (PPAR)-α expression plasmid and a peroxisome-proliferator-response element (PPRE) luciferase reporter plasmid in addition to a tk-Renilla luciferase plasmid to control for transfection efficiency. Cells were treated for 24 h as described in the text before harvesting and measuring luciferase activity. Concentrations of the treatments were as follows: 1 μM WY-14,643 (WY), 100 μM oleic acid, 40 μM compound C (CC), 500 μM AICAR, 1 mM metformin (Met). N = 4. *P < 0.05 compared with control; #P < 0.05 compared with WY; $P < 0.05 compared with WY + AICAR; &P < 0.05 compared with metformin + WY; δP < 0.05 compared with WY + CC.