HK2 and Hyperglycemia: These results raised the question of how the late phase of maternal hyperglycemia might upregulate HIF1A, HK2, and PFK. Although the molecular mechanism(s) that underlies this association remain understood, we cannot rule out the possibility that hyperglycemia might regulate HIF1A expression through altering cellular redox status since high glucose has been proposed to increase the cytosolic ratio of free NADH/NAD+ in diabetic patients (the phenomenon defined as pseudohypoxia) (Williamson et al., 1993; Caniggia et al., 2000; Song, Yang & Yan, 2019).