Interleukin-18 Activates Skeletal Muscle AMPK and Reduces Weight Gain and Insulin Resistance in Mice

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FIG. 5.
FIG. 5.

IL-18 increases fatty acid oxidation and AMPK signaling in skeletal muscle in vitro and ex vivo. Representative immunoblot and densitometric quantification of AMPK Thr172 in L6 cells (A) stimulated with 1 ng/mL and 10 ng/mL IL-18 for 30 min (n = 9/dose), representative immunoblot and densitometric quantification of ACCβ phosphorylation in L6 cells (B) stimulated with 1 ng/mL and 10 ng/mL IL-18 for 30 min (n = 9/dose), fatty acid oxidation (C) in isolated soleus muscle strips in the presence of IL-18 (100 ng/mL) or PBS (untreated [UT]) (n = 10/group), and representative immunoblot and densitometric quantification (D) of AMPK Thr172 phosphorylation in isolated soleus muscle strips in the presence of IL-18 (100 ng/mL) or PBS (UT) (n = 6/group). Results are presented as mean ± SEM. *P < 0.05; **P < 0.01 vs. control (UT). pACC, phosphorylated ACC; pAMPK, phosphorylated AMPK.

This Article

  1. Diabetes vol. 62 no. 9 3064-3074