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. 2016 Aug;16(3):162–179. doi: 10.17305/bjbms.2016.919

FIGURE 8.

FIGURE 8

Characterization of the insulin secretion defect in Bad−/− islets. (A) Perifused islets from Bad−/− mice (red) with 25 mM glucose secreted significantly less insulin compared with that of Bad+/+ islets (black). (B) Insulin secretion throughout the perifusion (min 0-40), first phase (min 8-15) and second phase (min 15-40). (C) Glucose-induced changes in ATP/ADP ratio in Bad+/+ and Bad−/− islets - 5.5 mM (black), 25 mM (blue). (D) Insulin secretion in response to glucose 5.5 mM and 25 mM, 10 mM σ-ketoisocaproate (KIC), 0.25 mM tolbutamide and carbachol. (E) GCK activity in homogenates of primary islets isolated from Bad+/+ (black) and Bad−/− mice (red). (F) Insulin secretion by Bad+/+ (black) and Bad−/− (red) islets perifused with incrementally increasing concentration of glucose. From Daniel NN, et al. Nature 2003;424:952-6.