Figure 7.

11-DHC effects are mediated through the GR. A: The GR antagonist RU486 prevents the suppressive effects of 11-DHC on glucose- and glucose + KCl–stimulated Ca²⁺ signals (mean ± SEM traces shown; n = 12–13 islets from four animals). B and C: As for A, but summary bar graphs showing that 11-DHC does not affect Ca²⁺ responses to glucose (B) or glucose + KCl (C) in RU486-treated islets. D: Representative maximum intensity projection images showing impaired Ca²⁺ rises in 11-DHC–treated islets, which can be reversed by using the GR antagonist RU486 (scale bar = 20 μm) (images cropped to show a single islet). E: RU486 blocks the effects of corticosterone on Ca²⁺ responses to glucose (n = 14–17 islets from six animals). F: As for E, but RU486 is unable to significantly affect Ca²⁺ responses to glucose + KCl in corticosterone-treated islets (n = 14–17 islets from six animals). 11-DHC and corticosterone were applied for 48 h at 200 nmol/L and 20 nmol/L, respectively. KCl was applied at 10 mmol/L. Unless otherwise stated, data are mean ± SD. *P < 0.05, **P < 0.01 by one-way ANOVA (Bonferroni post hoc test). Islets were pretreated with 1 μmol/L RU486. Con, control; Cort, corticosterone; G3, 3 mmol/L glucose; G17, 17 mmol/L glucose; max, maximum; min, minimum; NS, nonsignificant.