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. Author manuscript; available in PMC: 2013 Feb 1.
Published in final edited form as: Hepatology. 2011 Dec 29;55(2):437–446. doi: 10.1002/hep.24708

Figure 5. Pharmacological or genetic activation of AMPK prevents enhanced expression of Lpin1 and elevated lipid accumulation induced by ethanol.

Figure 5

(A) AML-12 cells were transiently transfected with expression plasmids for Lpin1-luciferase, along with or without expression plasmids for AMPKα312, control siRNA, or AMPKα siRNA (5 μg/each). Ethanol, AICAR (0.5 mM), or compound C (3μM) was then added. Cells then were harvested for assay of the Lpin1-luciferase activity. (B) AML-12 cells were transfected with AMPKα312, control siRNA, SREBP-1siRNA or nSREBP-1. Ethanol, AICAR (0.5 mM), or compound C (3μM) was then added. Seventy-two hours after transfection, qRT-PCR was used to estimate relative mRNA levels of lipin-1. All data are given as means±SD from at least 3–5 experiments. Means without a common letter differ, p< 0.05.