ArticleThe Journal of biological chemistry2011
Kinetic evidence that Glut4 follows different endocytic pathways than the receptors for transferrin and alpha2-macroglobulin.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Integrated analysis of the adipocyte plasma membrane proteome reveals KCC1 and PIT2 as novel insulin-responsive transporters.The Journal of biological chemistry · 2026Article
- Does GLUT4 Queue? A Mechanistic Mathematical Model for Insulin Response in Adipocytes.Bulletin of mathematical biology · 2025Article
- GLUT4 Trafficking and Storage Vesicles: Molecular Architecture, Regulatory Networks, and Their Disruption in Insulin Resistance.International journal of molecular sciences · 2025Review
- The Functions of SARS-CoV-2 Receptors in Diabetes-Related Severe COVID-19.International journal of molecular sciences · 2024Review
- High-throughput proteomics uncovers exercise training and type 2 diabetes-induced changes in human white adipose tissue.Science advances · 2023Article
- Benchmarking Thiolate-Driven Photoswitching of Cyanine Dyes.The journal of physical chemistry. B · 2023Article
- A high-content endogenous GLUT4 trafficking assay reveals new aspects of adipocyte biology.Life science alliance · 2023Article
- Knockout of syntaxin-4 in 3T3-L1 adipocytes reveals new insight into GLUT4 trafficking and adiponectin secretion.Journal of cell science · 2022Article
- 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
- GLUT4 Storage Vesicles: Specialized Organelles for Regulated Trafficking.The Yale journal of biology and medicine · 2019Review
- Thirty sweet years of GLUT4.The Journal of biological chemistry · 2019Review
- A high-throughput chemical-genetics screen in murine adipocytes identifies insulin-regulatory pathways.The Journal of biological chemistry · 2019Article
- Chemical biology probes of mammalian GLUT structure and function.The Biochemical journal · 2018Review
- Insulin differentially affects the distribution kinetics of amyloid beta 40 and 42 in plasma and brain.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Article
- Glut4 Is Sorted from a Rab10 GTPase-independent Constitutive Recycling Pathway into a Highly Insulin-responsive Rab10 GTPase-dependent Sequestration Pathway after Adipocyte Differentiation.The Journal of biological chemistry · 2016Article
- Age and its association with low insulin and high amyloid-β peptides in blood.Journal of Alzheimer's disease : JAD · 2016Article
- Rab5 activity regulates GLUT4 sorting into insulin-responsive and non-insulin-responsive endosomal compartments: a potential mechanism for development of insulin resistance.Endocrinology · 2014Article
- Reciprocal regulation of endocytosis and metabolism.Cold Spring Harbor perspectives in biology · 2014Review
- Insulin-regulated Glut4 translocation: membrane protein trafficking with six distinctive steps.The Journal of biological chemistry · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Insulin regulates glucose uptake through effects on the trafficking of the glucose transporter Glut4. To investigate the degree of overlap between Glut4 and the general endocytic pathways, the kinetics of trafficking of Glut4 and the receptors for transferrin (Tf) and α(2)-macroglobulin (α-2-M; LRP-1) were compared using quantitative flow cytometric assays. Insulin increased the exocytic rate constant (k(ex)) for both Glut4 and Tf. However, the k(ex) of Glut4 was 5-15 times slower than Tf in both basal and insulin-stimulated cells. The endocytic rate constant (k(en)) of Glut4 was also five times slower than Tf. Insulin did not affect the k(en) of either protein. In basal cells, the k(en) for α-2-M/LRP-1 was similar to Glut4 but 5-fold slower than Tf. Insulin increased k(en) for α-2-M/LRP-1 by 30%. In contrast, the k(ex) for LRP-1 was five times faster than Glut4 in basal cells, and insulin did not increase this rate constant. Thus, although there is overlap in the protein machineries/compartments utilized, the differences in trafficking kinetics indicate that Glut4, the Tf receptor, and LRP-1 are differentially processed both within the cell and at the plasma membrane. It has been reported that insulin decreases the k(en) of Glut4 in adipocytes. However, the effect of exocytosis on the "internalization" assays was not considered. Because it is counterintuitive, the effect of exocytosis on these assays is often overlooked in endocytosis studies. Using mathematical modeling and simulation, we show that the reported decrease in Glut4 k(en) can be entirely accounted for by the well established increase in Glut4 k(ex).
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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.