Glucose Transporter 1 in Health and Disease.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic and therapeutic concepts without systematic review methodology or new empirical human data.
PubMed 42494471 · doi:10.1002/mco2.70874
What was done
This narrative review synthesized the multidimensional regulatory networks of Glucose Transporter 1 (GLUT1) in physiological homeostasis and pathological conditions. The authors reviewed GLUT1's role in basal glucose transport across the blood-brain barrier, consequences of genetic haploinsufficiency, cancer-driven metabolic remodeling within the tumor microenvironment, and emerging precision therapeutic platforms such as glycan-functionalized nanocarriers, PROTACs, and engineered CAR-T cells.
What was found
The abstract provides a qualitative, mechanistic synthesis and reports no numerical data or effect sizes. It details how GLUT1 deficiency precipitates severe neurological dysfunction like Glut1 deficiency syndrome (Glut1DS), while oncogenic hyperactivation drives the Warburg effect, metabolic immune exclusion, and therapy resistance. It identifies normal-tissue toxicity as the primary barrier to systemic GLUT1 blockade.
Why it matters
The paper contextualizes GLUT1 as a critical hub linking tumor metabolism to immune evasion, providing a conceptual framework for precision delivery and targeted degradation approaches that avoid systemic toxicities.
Limits
As a narrative review, this paper presents theoretical and mechanistic syntheses rather than new human experimental data, clinical trial outcomes, or systematic meta-analytic findings. No specific sample sizes, search strategies, or quantitative metrics are reported in the abstract.
Cited by
- supports Glucose is the major fuel for human cells, especially brain cells, and directly affects brain function, mood, and energy levels.