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. 2017 Jan 23;66(4):948–959. doi: 10.2337/db16-0636

Figure 2.

Figure 2

Syn-2 deletion increases biphasic insulin secretion. A: Islet perifusion assays in WT and Syn-2–KO mice pancreatic islets (left) and corresponding AUCs of insulin release (right) stimulated by 16.7 mmol/L glucose and then with application of GLP-1 (10 nmol/L). Data are from six independent experiments. B: Islet perifusion assays of Syn-2–KO mouse islets for which Syn-2 expression is restored by Ad-Syn-2–EGFP infection (Supplementary Fig. 2A); corresponding AUCs are shown on the right. C: Representative recordings of ΔCm during of a train of 500-ms depolarizations from −70 to 0 mV in WT and Syn-2–KO β-cells. Changes in cell Cm for each pulse in D and cumulative changes in Cm normalized to basal cell Cm (fF/pF) in E during a train of 10 500-ms depolarizations in WT (n = 20 cells) and Syn-2–KO (n = 18 cells) β-cells. F: Summary of Cm evoked by the first two pulses (pulses 1 and 2 represent the RRP) and the next eight pulses (pulses 3–10 represent SG mobilization). n = 18–20 cells. Summary graphs shown as mean ± SEM. *P < 0.05.