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. 2011 Oct 17;60(11):2710–2719. doi: 10.2337/db11-0132

FIG. 4.

FIG. 4.

UCP2BKO islets display ROS-dependent enhanced GSIS. A: Measurement of GSIS over time in RIPCre and UCP2BKO islets by perifusion with varying concentrations of glucose (2.8, 11, and 16.7 mmol/L). Areas under the curve (AUC) are shown for 11 mmol/L glucose (B) and 16.7 mmol/L glucose (C). n = 6. *P < 0.05. Measurement of GSIS after manipulation of intracellular ROS levels in RIPCre (D) and UCP2BKO (E) islets using the pro-oxidant DEM (5 mmol/L) or the antioxidant NAC (0.2 mmol/L) by static incubation. Islets were preincubated in 2.8 mmol/L glucose for 1 h (±5 mmol/L DEM or 0.2 mmol/L NAC), followed by 30-min incubation in 2.8 or 16.7 mmol/L glucose (±5 mmol/L DEM or 0.2 mmol/L NAC). Insulin secretion was measured in nanograms of insulin per islet. n = 4. *P < 0.05. F: Measurement of GSIS in human islets in the presence or absence of 50 µmol/L genipin. Human islets were subjected to a similar static secretion protocol as mouse islets. Acute preincubation in genipin, a known UCP2 inhibitor, stimulates insulin secretion from human islets. n = 3 independent experiments. **P < 0.01. LG, low glucose; HG, high glucose. The error bars show the SEM.