ArticleMolecular biology of the cell2000
Insulin recruits GLUT4 from specialized VAMP2-carrying vesicles as well as from the dynamic endosomal/trans-Golgi network in rat adipocytes.
Article in Molecular biology of the cell, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 74 citations in OpenAlex.
- Progress in Understanding the Regulation of Glucose and Fructose Metabolism.Annual review of nutrition · 2025Review
- Influence of Protein Carbonylation on Human Adipose Tissue Dysfunction in Obesity and Insulin Resistance.Biomedicines · 2022Article
- Isolation and Proteomics of the Insulin Secretory Granule.Metabolites · 2021Review
- Structure, function and regulation of mammalian glucose transporters of the SLC2 family.Pflugers Archiv : European journal of physiology · 2020Review
- BAG6 contributes to glucose uptake by supporting the cell surface translocation of the glucose transporter GLUT4.Biology open · 2020Article
- Chemical biology probes of mammalian GLUT structure and function.The Biochemical journal · 2018Review
- Suppression of VAMP2 Alters Morphology of the Tegument and Affects Glucose uptake, Development and Reproduction of Schistosoma japonicum.Scientific reports · 2017Article
- TUSC5 regulates insulin-mediated adipose tissue glucose uptake by modulation of GLUT4 recycling.Molecular metabolism · 2015Article
- PKA-independent cAMP stimulation of white adipocyte exocytosis and adipokine secretion: modulations by Ca2+ and ATP.The Journal of physiology · 2014Article
- Development of a quantitative Correlative Light Electron Microscopy technique to study GLUT4 trafficking.Protoplasma · 2014Article
- Expression of Glucose Transporter 4 (GLUT4) is Increased by Cinnamaldehyde in C2C12 Mouse Muscle Cells.Iranian Red Crescent medical journal · 2014Article
- Single point mutations result in the miss-sorting of Glut4 to a novel membrane compartment associated with stress granule proteins.PloS one · 2013Article
- Myo1c binding to submembrane actin mediates insulin-induced tethering of GLUT4 vesicles.Molecular biology of the cell · 2012Article
- GLUT4 exocytosis.Journal of cell science · 2011Review
- Loss of AS160 Akt substrate causes Glut4 protein to accumulate in compartments that are primed for fusion in basal adipocytes.The Journal of biological chemistry · 2011Article
- Dual-mode of insulin action controls GLUT4 vesicle exocytosis.The Journal of cell biology · 2011Article
- Kinetic evidence that Glut4 follows different endocytic pathways than the receptors for transferrin and alpha2-macroglobulin.The Journal of biological chemistry · 2011Article
- Regulation of glucose transporter 4 translocation by the Rab guanosine triphosphatase-activating protein AS160/TBC1D4: role of phosphorylation and membrane association.Molecular endocrinology (Baltimore, Md.) · 2008Article
- The GLUT4 code.Molecular endocrinology (Baltimore, Md.) · 2008Review
- Ins (endocytosis) and outs (exocytosis) of GLUT4 trafficking.Current opinion in cell biology · 2007Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin treatment of fat cells results in the translocation of the insulin-responsive glucose transporter type 4, GLUT4, from intracellular compartments to the plasma membrane. However, the precise nature of these intracellular GLUT4-carrying compartments is debated. To resolve the nature of these compartments, we have performed an extensive morphological analysis of GLUT4-containing compartments, using a novel immunocytochemical technique enabling high labeling efficiency and 3-D resolution of cytoplasmic rims isolated from rat epididymal adipocytes. In basal cells, GLUT4 was localized to three morphologically distinct intracellular structures: small vesicles, tubules, and vacuoles. In response to insulin the increase of GLUT4 at the cell surface was compensated by a decrease in small vesicles, whereas the amount in tubules and vacuoles was unchanged. Under basal conditions, many small GLUT4 positive vesicles also contained IRAP (88%) and the v-SNARE, VAMP2 (57%) but not markers of sorting endosomes (EEA1), late endosomes, or lysosomes (lgp120). A largely distinct population of GLUT4 vesicles (56%) contained the cation-dependent mannose 6-phosphate receptor (CD-MPR), a marker protein that shuttles between endosomes and the trans-Golgi network (TGN). In response to insulin, GLUT4 was recruited both from VAMP2 and CD-MPR positive vesicles. However, while the concentration of GLUT4 in the remaining VAMP2-positive vesicles was unchanged, the concentration of GLUT4 in CD-MPR-positive vesicles decreased. Taken together, we provide morphological evidence indicating that, in response to insulin, GLUT4 is recruited to the plasma membrane by fusion of preexisting VAMP2-carrying vesicles as well as by sorting from the dynamic endosomal-TGN system.
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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.