ReviewEMBO reports2005
Glucose transporter 4: cycling, compartments and controversies.
Review in EMBO reports, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
82 citing papers in PubMed, 228 citations in OpenAlex.
- HDL-Cholesterol and Triglycerides Dynamics: Essential Players in Metabolic Syndrome.Antioxidants (Basel, Switzerland) · 2025Review
- Exploring Morphological and Molecular Properties of Different Adipose Cell Models: Monolayer, Spheroids, Gellan Gum-Based Hydrogels, and Explants.Macromolecular bioscience · 2025Article
- Genetic deletion of zinc transporter ZnTFrontiers in molecular neuroscience · 2024Article
- Metabolic adaptations in pressure overload hypertrophic heart.Heart failure reviews · 2024Review
- Effects of Polyphenols on Glucose-Induced Metabolic Changes in Healthy Human Subjects and on Glucose Transporters.Molecular nutrition & food research · 2022Review
- Cardiac metabolic remodelling in chronic kidney disease.Nature reviews. Nephrology · 2022Review
- Persistent high glucose induced EPB41L4A-AS1 inhibits glucose uptake via GCN5 mediating crotonylation and acetylation of histones and non-histones.Clinical and translational medicine · 2022Article
- Peripheral versus central insulin and leptin resistance: Role in metabolic disorders, cognition, and neuropsychiatric diseases.Neuropharmacology · 2022Review
- Rapid Regulation of Glutamate Transport: Where Do We Go from Here?Neurochemical research · 2022Review
- Intranasal insulin and orexins to treat age-related cognitive decline.Physiology & behavior · 2021Review
- Review
- Insulin signaling in health and disease.The Journal of clinical investigation · 2021Review
- Effects of Polyphenols on Insulin Resistance.Nutrients · 2020Review
- GLUT4 Storage Vesicles: Specialized Organelles for Regulated Trafficking.The Yale journal of biology and medicine · 2019Review
- Article
- Apolipoprotein A-I enhances insulin-dependent and insulin-independent glucose uptake by skeletal muscle.Scientific reports · 2019Article
- The carboxy-terminal region of the TBC1D4 (AS160) RabGAP mediates protein homodimerization.International journal of biological macromolecules · 2017Article
- EsGLUT4 and CHHBP are involved in the regulation of glucose homeostasis in the crustaceanBiology open · 2017Article
- Absence of IQGAP1 Protein Leads to Insulin Resistance.The Journal of biological chemistry · 2017Article
- MicroRNA-29a induces insulin resistance by targeting PPARδ in skeletal muscle cells.International journal of molecular medicine · 2016Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin promotes glucose uptake into muscle and adipose tissues through glucose transporter 4 (GLUT4). In unstimulated cells, rapid endocytosis, slow exocytosis and dynamic or static retention cause GLUT4 to concentrate in early recycling endosomes, the trans-Golgi network and vesicle-associated protein 2-containing vesicles. The coordinated action of phosphatidylinositol 3-kinase effectors, protein kinase Akt, atypical protein kinase C (aPKC) and Akt substrate of 160-kDa (AS160), regulates the GLUT4 cycle by affecting its translocation, fusion with the plasma membrane, internalization and sorting. We review the evidence that supports such cycling, evaluate current models proposing static or dynamic retention, and highlight how distinct steps of GLUT4 transport are regulated by insulin signals. In particular, fusion seems to be regulated by aPKC (via munc18) and Akt (via syntaxin4-interacting protein (synip)). AS160 participates in GLUT4 intracellular retention, and possibly fusion, through candidate ras-related GTP-binding protein (Rab)2, Rab8, Rab10 and/or Rab14. The localization of the insulin-sensitive GLUT4 compartment and the precise target of insulin-derived signals remain open for future investigation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.