PKC and Rab13 mediate Ca²⁺ signal-regulated GLUT4 traffic.

Exercise/muscle contraction increases cell surface glucose transporter 4 (GLUT4), leading to glucose uptake to regulate blood glucose level. Elevating cytosolic Ca²⁺ mediates this effect, but the detailed mechanism is not clear yet. We used calcium ionophore ionomycin to raise intracellular cytosolic Ca²⁺ level to explore the underlying mechanism. We showed that in L6 myoblast muscle cells stably expressing GLUT4myc, ionomycin increased cell surface GLUT4myc levels and the phosphorylation of AS160, TBC1D1. and but not and inhibited the ionomycin-increased cell surface GLUT4myc level. siduanyu1531θ inhibited the phosphorylation of AS160 and TBC1D1 induced by ionomycin. siduanyu1531α and siduanyu1531θ prevented ionomycin-inhibited endocytosis of GLUT4myc. but not siduanyu1531α inhibited ionomycin-stimulated exocytosis of GLUT4myc. siRab13 but not siRab8a, siRab10 and siRab14 inhibited the exocytosis of GLUT4myc promoted by ionomycin. In summary, ionomycin-promoted exocytosis of GLUT4 is partly reversed by siduanyu1531θ, whereas ionomycin-inhibited endocytosis of GLUT4 requires both siduanyu1531α and and contribute to ionomycin-induced phosphorylation of AS160 and TBC1D1. Rab13 is required for ionomycin-regulated GLUT4 exocytosis.

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