ArticleAmerican journal of physiology. Endocrinology and metabolism2012
Insulin stimulates fusion, but not tethering, of GLUT4 vesicles in skeletal muscle of HA-GLUT4-GFP transgenic mice.
Article in American journal of physiology. Endocrinology and metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- Intravenous regular insulin is an efficient and safe procedure for obtaining high-quality cardiacJournal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2022Trial
- Trial
- Exofacial Epitope-Specific Antibodies Detect GLUT4 Translocation in Adult Human, Rat, and Mouse Skeletal Muscle.Diabetes · 2026Article
- Does GLUT4 Queue? A Mechanistic Mathematical Model for Insulin Response in Adipocytes.Bulletin of mathematical biology · 2025Article
- GLUT4 localisation with the plasma membrane is unaffected by an increase in plasma free fatty acid availability.Lipids in health and disease · 2024Article
- Microtubule-mediated GLUT4 trafficking is disrupted in insulin-resistant skeletal muscle.eLife · 2023Article
- GLUT4 translocation and dispersal operate in multiple cell types and are negatively correlated with cell size in adipocytes.Scientific reports · 2022Article
- GLUT4 On the move.The Biochemical journal · 2022Article
- AMPK-mediated phosphorylation enhances the auto-inhibition of TBC1D17 to promote Rab5-dependent glucose uptake.Cell death and differentiation · 2021Article
- Luseogliflozin, a SGLT2 Inhibitor, Does Not Affect Glucose Uptake Kinetics in Renal Proximal Tubules of Live Mice.International journal of molecular sciences · 2021Article
- Olive Leaf Polyphenols (OLPs) Stimulate GLUT4 Expression and Translocation in the Skeletal Muscle of Diabetic Rats.International journal of molecular sciences · 2020Article
- Prior exercise in humans redistributes intramuscular GLUT4 and enhances insulin-stimulated sarcolemmal and endosomal GLUT4 translocation.Molecular metabolism · 2020Article
- Article
- The cell biology of systemic insulin function.The Journal of cell biology · 2018Review
- Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy.Journal of visualized experiments : JoVE · 2017Article
- Cell-autonomous adiposity through increased cell surface GLUT4 due to ankyrin-B deficiency.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Drosophila as a Model for Diabetes and Diseases of Insulin Resistance.Current topics in developmental biology · 2017Review
- Ankyrin-B metabolic syndrome combines age-dependent adiposity with pancreatic β cell insufficiency.The Journal of clinical investigation · 2015Article
- Visualization and quantitation of GLUT4 translocation in human skeletal muscle following glucose ingestion and exercise.Physiological reports · 2015Article
- Quantitative immunofluorescence microscopy of subcellular GLUT4 distribution in human skeletal muscle: effects of endurance and sprint interval training.Physiological reports · 2014Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 4 countries.
Funding
Abstract
Insulin regulates glucose uptake into fat and muscle by modulating the subcellular distribution of GLUT4 between the cell surface and intracellular compartments. However, quantification of these translocation processes in muscle by classical subcellular fractionation techniques is confounded by contaminating microfibrillar protein; dynamic studies at the molecular level are almost impossible. In this study, we introduce a muscle-specific transgenic mouse model in which HA-GLUT4-GFP is expressed under the control of the MCK promoter. HA-GLUT4-GFP was found to translocate to the plasma membrane and T-tubules after insulin stimulation, thus mimicking endogenous GLUT4. To investigate the dynamics of GLUT4 trafficking in skeletal muscle, we quantified vesicles containing HA-GLUT4-GFP near the sarcolemma and T-tubules and analyzed insulin-stimulated exocytosis at the single vesicle level by total internal reflection fluorescence and confocal microscopy. We found that only 10% of the intracellular GLUT4 pool comprised mobile vesicles, whereas most of the GLUT4 structures remained stationary or tethered at the sarcolemma or T-tubules. In fact, most of the insulin-stimulated exocytosis emanated from pretethered vesicles, whereas the small pool of mobile GLUT4 vesicles was not significantly affected by insulin. Our data strongly suggest that the mobile pool of GLUT4 vesicles is not a major site of insulin action but rather locally distributed. Most likely, pretethered GLUT4 structures are responsible for the initial phase of insulin-stimulated exocytosis.
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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.