Figure 2.

Glucocorticoids impair VDCC function despite preserved β-cell identity and metabolism. A–F: Expression of mRNA for the β-cell maturity markers Pdx-1 (A–C) and Nkx6.1 (D–F) are similar in control and 11-DHC/corticosterone-treated islets (n = 4–7 animals, 48 h). G: Mean ± SEM traces showing no effect of glucocorticoids on maximal ATP/ADP responses to glucose measured using the biosensor Perceval. H: As for G, but summary bar graph showing the amplitude of ATP/ADP rises (n = 7 islets from four animals). I: 11-DHC and corticosterone reduce VDCC conductance as shown by the voltage-current relationship (n = 4 animals). J: As for I, but representative Ca²⁺ current traces. K–P: Expression levels of the VDCC α/β-subunits Cacna1c (K and L), Cacnb2 (M and N), and Cacna1d (O and P) are not significantly altered by 11-DHC or corticosterone (n = 4–6 animals, 48 h). Corticosterone was applied at 20 nmol/L for 48 h. Unless otherwise stated, data are mean ± SD. *P < 0.05, **P < 0.01 for 11-DHC vs. control; #P < 0.05, ##P < 0.01 for corticosterone vs. control (NS, nonsignificant) by Student t test, Student paired t test, or one-way ANOVA (Bonferroni post hoc test). Cort, corticosterone; G3, 3 mmol/L glucose; G17, 17 mmol/L glucose.