Jwa Kum Whan Attenuates Nonalcoholic Fatty Liver Disease by Modulating Glucose Metabolism and the Insulin Signaling Pathway

Figure 3

Effects of JKW on proteins related to insulin signaling and energy metabolism in HepG2 cells. (a) After starving HepG2 cells for 24 h, they were cotreated with FFAs (1 mM) and JKW (10 or 25 μg/mL) for 24 h. Cells were incubated with 50 nM of insulin for 30 min before harvest. Relative IRS-1, PI3K, and AKT levels, which represent insulin signaling pathways, were assessed by dividing the expressions of phosphorylated proteins by those of corresponding nonphosphorylated proteins. (b) Relative levels of energy metabolism-related proteins (AMPK, CPT-1, C/EBPα, and PPARγ) were determined by normalizing protein expressions versus β-actin protein (or phosphorylated AMPK) expression. Results are expressed as the means ± SDs of three independent experiments. < 0.05 versus untreated controls. < 0.05 and < 0.01 versus FFA-treated controls.

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