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. 2011 Jun 6;108(25):10162–10167. doi: 10.1073/pnas.1019268108

Fig. 2.

Fig. 2.

GLUT4 translocation and FoxO1 nuclear exclusion display distinct sensitivities to insulin. (A) Insulin-dose response for HA-GLUT4-GFP translocation and FoxO1 nuclear exclusion. Each point is the mean ± SEM, n≥5. (B) Immunoblot of insulin signaling intermediates in adipocytes stimulated with insulin for 30 min. (C) Densitometry analyses of experiments like those shown in B. Each point is mean ± SEM, n = 3. Values were normalized to that of 10 nM insulin treated cells. (D) ED50s for insulin-induced GLUT4 plasma membrane translocation, FoxO1 nuclear exclusion, and Akt, TBC1D4, and FoxO1 phosphorylation. The values were derived from the data in A and C using a dose-response logistic curve fit. (E) Insulin-dose response for HA-GLUT4-GFP translocation and FoxO1-GFP nuclear exclusion in control adipocytes and adipocytes exposed to chronic hyperinsulinemia (CHI). Each point is the mean ± SEM, n≥3.