Abstract: Abstract Objective: To study the role of Ca2＋/Calmodulin- dependent protein kinase II (CaMK II) in the mechanism of contract-stimulated glucose transport 4 translocation in skeletal muscle cells. Methods: C2C12GLUT4myc myotubes were divided into two groups with or without carbachol (acetylcholine receptor agonist) treatment. CaMK II inhibitor KN93 or KN62 was added to the medium prior to treatment, respectively. Then cell surface levels of GLUT4myc were measured by enzyme linked immunosorbent assay (ELISA). The phosphorylation of CaMK II was detected by immunoblotting after pre-incubation with KN93 before treatment. Results: Carbachol increased phosphorylation of CaMK II which was reduced by KN93. KN93 and KN62 inhibited the gain of cell surface GLUT4myc induced by Cch. Conclusion: CaMK II is the downstream signal of Ca2＋ and mediates contraction-stimulated GLUT4myc traffic in skeletal muscle cells.

Key words: CaMK II, muscle, skeletal, GLUT4, carbachol, contraction