ABSTRACT
Glucose transporters (GLUTs) encoded by the solute carrier family 2 (SLC2) gene belong to the major facilitator superfamily (MFS) and are responsible for the transmembrane transport of glucose in the body. As the earliest discovered member of the GLUTs, glucose transporter 1 (GLUT1) is mainly found in the blood-brain barrier and erythrocyte membrane, and plays an important role in maintaining stable blood glucose concentration and energy supply to the brain. The transmembrane transport capacity of GLUT1 is not only related to the gene expression of SLC2 A1 on the cellular membrane, but also to the transport kinetic regulation of GLUT1. Generally, SLC2 A1 expression is regulated at the transcriptional, post-transcriptional, translational and post-translational levels, and the transport kinetics regulation includes a series of GLUT1 inhibitors, such as intramembrane glycan-binding site inhibitor, extramembrane glycan-binding site inhibitor, adenosine-binding effect inhibitors and the highly selective inhibitor BAY-876. SLC2 A1 gene deletions and mutations can cause embryonic mortality and GLUT1 deficiency syndrome. In contrast, abnormally high SLC2 A1 expression is associated with various diabetic complications (e. g. diabetic retinopathy and diabetic nephropathy), neurocognitive impairment and tumorigenesis. In this paper, the structure, function, expression and activity regulation of GLUT1 and its relationship with diseases were reviewed to provide a reference for the GLUT1-related clinical research and drug development.