Endothelial cells (ECs) are highly glycolytic and generate most of their energy via the breakdown of glucose to lactate. The primary role of ECs is to allow the transport of glucose to its surrounding tissues.
GLUT1 (glucose transporter isoform 1/Slc2a1) is known to be highly expressed in ECs of the central nervous system (CNS) and is often implicated in blood-brain barrier (BBB) dysfunction, but whether and how GLUT1 controls EC metabolism and function is poorly understood. In this study, the role of GLUT1 was evaluated in endothelial function and metabolism during adult BBB and postnatal CNS development. Deleting GLUT1 from the developing postnatal retinal endothelium, lowers vascular outgrowth and reduces the retinal EC proliferation without affecting the number of tip cells. In contrast, in the brain, we observed a lower number of tip cells and reduced brain EC proliferation, indicating that within the CNS, organotypic differences in EC metabolism exist.
In conclusion, GLUT1 is the primary glucose transporter in ECs and becomes uncoupled from glycolysis during quiescence in a Notch-dependent manner. It is crucial for developmental CNS angiogenesis and adult CNS homeostasis but does not affect BBB barrier function. Taken together, we show that GLUT1 is the primary glucose transporter in ECs and is required for EC glycolysis.
Ref: https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.119.316463
