Figure 4.

Model of the proposed mechanism of CaMKII-dependent memory formation in pancreatic ß-cells. In low glucose concentrations (2.8 mM), control islets exhibit basal insulin secretion. Islets from the glucose pulse group show, even 24 h after the last high glucose pre-treatment, an increase in acute glucose-induced insulin secretion. This is due to the fact that ß-cells in the pulse group have increased expression of GCK, calcium channels, and phosphorylation of CaMKII. When exposed to high glucose, islets from the group control increase insulin secretion because of the increased glycolytic flux through GCK and elevated ATP production. ß-cells previously exposed to high glucose pulses have higher levels of GCK, calcium channel, Calcium influx, CaMKII phosphorylation, and therefore respond with higher insulin secretion to acute glucose.