A surprising finding of the study was that intracellular glucose decreased with extracellular hyperglycemia. This was associated with an increase in glycolysis (12) consistent with our previous observations, glycogen synthesis, and potentially other glucose utilization pathways such as the polyol pathway. Interestingly, glycogen synthase was stimulated by hyperglycemia in myoblasts but only when glycogen stores were depleted. The calculated glycogen content in our cells was ~10 times lower than that reported for glucose-starved myoblasts. Thus, it is possible that hyperglycemia also stimulates glycogen synthase in airway cells (14). BrPy increased intracellular glucose concentration. As HKII was reported to respond rapidly to changes in external glucose, we propose that HKII is key in directing the fate of glucose in these cells (17). However, intracellular concentration of glucose remained low compared with the external glucose concentration. This, together with the finding that only 25% of cellular hexokinase activity was inhibited by BrPy, indicates roles for hexokinase I and III in maintaining low intracellular glucose concentration in airway cells.