Figure 6. Glucose infusion and intermittent hypoxia increased pancreatic β-cell replication.

A, representative islets stained for BrdU and insulin show glucose-induced and hypoxia-induced replication. Insets: high magnification confirms BrdU-positive nuclei belong to insulin-positive cells. Scale bars, 20 μm. B, mean percentage β-cell replication during intermittent air exposure (saline, n = 9; glucose n = 10) and intermittent hypoxia exposure (saline, n = 9; glucose n = 9). Statistical difference determined by one-way ANOVA and Dunnett's post hoc assessment relative to the saline + intermittent air control group are shown above bars. Analysis by two-way ANOVA revealed a significant effect of infusion (glucose > saline; P < 0.05), no effect of intermittent hypoxia, but a significant interaction (glucose infusion reduced the rate of replication due to intermittent hypoxia exposure; P < 0.025). C, mean β-cell size during intermittent air exposure and intermittent hypoxia exposure (sample size same as B). D, mean changes in β-cells positive for TUNEL during intermittent air exposure and intermittent hypoxia exposure (sample size same as B). One-way ANOVA showed a trend for statistical significance (P = 0.085) and Dunnett's post hoc assessment showed an increase in apoptosis in the glucose + intermittent hypoxia group relative to the saline + intermittent air control group (P = 0.032). Analysis by two-way ANOVA revealed a significant effect of exposure (intermittent hypoxia > intermittent air; P < 0.05), but no effect of glucose infusion and no interaction. E, mean percentage β-cells that were pyknotic during intermittent air exposure and intermittent hypoxia exposure (sample size same as B). Sal + IA, saline infusion and intermittent air exposure; Glu + IA, glucose infusion and intermittent air exposure; Sal + IH, saline infusion and intermittent hypoxia exposure; Glu + IH, glucose infusion and intermittent hypoxia exposure.