Solute carrier family 2, facilitated glucose transporter member 1 (GLUT1) and Solute carrier family 2, facilitated glucose transporter member 3 (GLUT3) (GLUT1 and GLUT3)

Glucose transporters GLUT1 and GLUT3 are key members of the solute carrier family 2 (SLC2A) that facilitate the passive diffusion of glucose across plasma membranes [1.1.1, 1.1.3]. GLUT1 is ubiquitously expressed and serves as the primary transporter responsible for glucose delivery across the blood-brain barrier, while GLUT3 is predominantly found in neurons and possesses a high affinity for glucose to meet high metabolic demands [1.1.4, 1.3.3]. In many cancers, these transporters are significantly upregulated to facilitate the increased glucose consumption required for rapid proliferation, a phenomenon known as the Warburg effect [1.2.2, 1.2.3]. Consequently, GLUT1 and GLUT3 are prominent therapeutic targets in oncology, with various small-molecule inhibitors like BAY-876 and WZB117 being developed to disrupt tumor energy metabolism [1.3.2, 1.4.2]. Beyond cancer, mutations in the SLC2A1 gene cause GLUT1 deficiency syndrome, leading to severe neurological symptoms due to impaired brain glucose supply [1.1.2, 1.4.1]. Conversely, reduced expression of both GLUT1 and GLUT3 has been implicated in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease [1.2.1, 1.3.4]. Therapeutic interventions targeting these transporters must carefully balance efficacy against the risk of systemic hypoglycemia and neuroglycopenia [1.4.1]. Additionally, GLUT1 serves as a receptor for human T-cell leukemia viruses (HTLV-I and II), adding another layer to its biological significance [1.1.2].

Other names

SLC2A1SLC2A3Glucose transporter type 1Glucose transporter type 3Erythrocyte glucose transporterNeuron-specific glucose transporterHepG2 glucose transporterSolute carrier family 2 member 1Solute carrier family 2 member 3

Inhibition of facilitated glucose transport, blockade of glycolytic metabolism, and chemo-radiosensitization of tumor cells [1.2.3, 1.3.2].