Consider a slightly different narrative.In the early 2000s America was in the grips of savings-glut-like conditions.
In resting conditions, GLUT 2 is the predominant transporter for glucose in hepatic parenchymal cells [ 24, 31].
Under hypoxic conditions, Glut-1 expression can be enhanced by HIF-1α [ 19].
This pattern and agreement reflects their interrelated role in the glycolytic pathway under hypoxic conditions, GLUT-1 for glucose import and MCT4 for lactate export.
The proliferation of clones of cells with upregulated GLUT-1 under physiologic conditions is consistent with our hypothesis that this phenotype confers a proliferative advantage.
Previous studies have suggested that, along with a decrease in GLUT-4 expression [67], [68], conditions of obesity and insulin resistance can be accompanied by increased expression of the constitutive glucose transporter GLUT-1 in adipose tissue (e.g., reference [69]).
As GLUTs are expressed in control conditions and after stroke, transport of dehydroascorbate into the brain could be found with and without stroke in our present study and previous studies by other investigators [11], [13].
The expression of GLUT-1 increased under nonaerobic conditions, inducing a metabolic shift towards glycolysis.
This observation is in agreement with studies in other cells where high glucose, glucose re-feeding after deprivation or diabetic conditions led to GLUT-1 routing to intracellular compartments followed by lysosomal degradation [ 26, 27, 34, 35].
The same group reported that ALDHdim EPCs, but not ALDHbr EPCs, from human UCB upregulated hypoxia-inducible factor proteins as well as VEGF, CXCR4, and GLUT-1 mRNAs under hypoxic conditions [ 22].
