Exercise, GLUT4, and skeletal muscle glucose uptake.
Level 5 - mechanism / opinion, no new human data
Narrative review of molecular mechanisms without systematic search methodology
PubMed 23899560 · doi:10.1152/physrev.00038.2012
What was done
This narrative review summarizes the physiological and molecular mechanisms governing exercise-induced skeletal muscle glucose uptake, concentrating on GLUT4 translocation, acute intracellular signaling cascades, and the transcriptional regulation of GLUT4 expression.
What was found
The abstract reports no quantitative values or statistical comparisons. It outlines that acute contraction mobilizes GLUT4 to the plasma membrane and T-tubules via proximal signaling (AMPK, Ca2+, NOS) and distal regulators (GTPases, Rab, SNARE proteins, and cytoskeletal elements). In addition, exercise training upregulates GLUT4 transcription through AMPK and CaMKII signaling via the HDAC4/5-MEF2 axis and MEF2-GEF interactions, leading to HDAC4/5 nuclear export and histone hyperacetylation at the GLUT4 promoter.
Why it matters
Understanding the molecular cascades by which physical activity drives GLUT4 translocation and expression clarifies how exercise enhances insulin sensitivity, glucose disposal, and glycogen storage in both healthy and clinical populations.
Limits
As a narrative review, the abstract provides no systematic literature search criteria, study counts, sample sizes, or quantitative effect sizes. The relative contributions of findings derived from human trials versus animal or in vitro models are not specified.
Cited by
- supports Skeletal muscle contraction triggers the translocation of GLUT4 glucose transporters to the muscle cell membrane independently to facilitate glucose uptake.