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. Author manuscript; available in PMC: 2012 Sep 1.
Published in final edited form as: Free Radic Biol Med. 2010 Dec 13;51(5):993–999. doi: 10.1016/j.freeradbiomed.2010.12.005

Figure 1.

Figure 1

Schematic representation of the overproduction of oxidants from NADPH oxidase and mitochondrial sources in mammalian skeletal muscle, with subsequent enhanced engagement of p38 MAPK and other stress-activated kinases, including JNK, GSK-3, IKKβ, and others, associated with diminished insulin-stimulated insulin signaling and reduced glucose transport activity.