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. 2016 Jul 8;11(7):e0159191. doi: 10.1371/journal.pone.0159191

Fig 2. APL improved palmitate -induced insulin resistance through activating AMPK in skeletal muscle myotubes.

Fig 2

(A). Differentiated L6 cells were untreated or pretreated with palmitate (PA,0.75 mM) for 16 h, then incubated with 10 μM APL for 24 h in the presence or absence of insulin (100 nM). Western blots detected p-AMPK and AMPK (B) Differentiated L6 cells were pretreated with palmitate (PA,0.75 mM) for 16 h, then incubated with 1, 5 or 10 μM APL for another 24 h in the presence of insulin (100 nM). Western blots detected p-AMPK and AMPK. (C) Differentiated L6 cells were pretreated with palmitate (PA,0.75 mM) for 16 h, then incubated with (10 μM) of APL for 6, 12 or 24 h in the presence of insulin (100 nM). Western blots detected p-AMPK and AMPK. (D) Differentiated L6 cells were pretreated with palmitate (PA,0.75 mM) for 16 h, then with CC (10 μM) for 1 h or transfection with AMPK siRNA for 24 h,respectively, following by treated with 10 μM APL for 24 h in the presence or absence of insulin (100 nM). Total L6 cell lysates were used for western blots. (E) Differentiated L6 cells were treated as described in (D). Cells were collected and 2-NBDG glucose uptake was assessed. Values are means ± SEM. n = 3, ap < 0.05 palmitate -treated group; bp < 0.05 versus APL and palmitate co-treated group. All results are representative western blots of three independent experiments with similar results.