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. 2013 Aug 15;62(9):3064–3074. doi: 10.2337/db12-1095

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© 2013 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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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.