Molecular biology of mammalian glucose transporters.
Level 5 - mechanism / opinion, no new human data
Narrative review of basic molecular biology and bench research without human clinical trials.
PubMed 2407475 · doi:10.2337/diacare.13.3.198
What was done
This narrative review summarizes the molecular cloning, tissue distribution, physiological functions, gene structure, and chromosomal mapping of human sodium-glucose cotransporters and five facilitative glucose transporter isoforms (GLUT1 through GLUT5) based on basic science literature.
What was found
The abstract reports qualitative mechanistic descriptions rather than numerical trial data. Key findings include: - Sodium-glucose cotransporters drive glucose uptake against concentration gradients in the small intestine and kidney. - Five functional facilitative transporter cDNAs were identified: GLUT1 (erythrocytes) and GLUT3 (brain) mediate constitutive/basal transport; GLUT2 (liver, intestine, kidney, beta-cells) mediates bidirectional transport and glucose sensing; GLUT4 (muscle, fat) translocates in response to insulin; and GLUT5 is enriched in the small intestine. - Exon-intron organization was defined for human GLUT1, GLUT2, and GLUT4, with chromosomal localization and restriction-fragment-length polymorphisms identified across these gene loci.
Why it matters
This work consolidates the foundational molecular architecture of mammalian glucose transport, delineating how distinct transporter isoforms coordinate basal, active, and insulin-dependent glucose homeostasis.
Limits
The abstract provides a descriptive overview without reporting quantitative kinetic parameters, experimental sample sizes, methodological details, or clinical comparative data.
Cited by
- supports Most glucose uptake into the brain does not require insulin, whereas glucose uptake into skeletal muscle is insulin-dependent.