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. 2017 Dec 4;67(2):278–290. doi: 10.2337/db16-1356

Figure 3.

Figure 3

Insulin secretion from islets is maintained in the face of excess glucocorticoid. A: Basal, glucose-stimulated, and glucose + KCl–stimulated insulin secretion is unaffected after 48-h treatment of mouse islets with either 11-DHC or corticosterone (n = 5 animals). B–D: Quantitative real-time PCR analysis of Ins1 mRNA expression shows no significant changes in response to 11-DHC 20 nmol/L (B), 11-DHC 200 nmol/L (C), or corticosterone (D) (n = 4–7 animals). E: Total insulin content is unaffected by 11-DHC or corticosterone (n = 3 animals). F: Basal, glucose-stimulated, and glucose + KCl–stimulated insulin secretion is unaffected after 48-h treatment of human islets with either cortisone 200 nmol/L or cortisol 20 nmol/L (n = 3 donors). G: As for F, but stimulation index to better account for differences in basal secretion between islet batches from the various isolation centers. Corticosterone was applied at 20 nmol/L for 48 h. KCl was applied at 10 mmol/L. Unless otherwise stated, data are mean ± SD or range. *P < 0.05, **P < 0.01 by Student t test, one-way ANOVA (Bonferroni post hoc test), or two-way ANOVA. G3, 3 mmol/L glucose; G17, 17 mmol/L glucose; NS, nonsignificant.