Minireview: Recent Developments in the Regulation of Glucose Transporter-4 Traffic: New Signals, Locations, and Partners
Abstract
Glucose transporter (GLUT) 4 is the major glucose transporter of muscle and adipose cells, exquisitely regulated by insulin through posttranslational events. Twenty years after the seminal observations that GLUT4 levels rapidly rise at the plasma membrane (PM) and drop in endomembranes in response to an acute insulin challenge, we are still mapping the intracellular traffic of the transporter and the regulatory events that insulin unleashes. Newly synthesized GLUT4 enters an insulin-responsive compartment aided by GGA2 (an Arf-binding protein). In cultured adipocytes and myocytes, GLUT4 concentrates in a perinuclear pole through participation of microtubules and the EHD1 Eps15 homology domain-containing protein 1. In the absence of stimuli, GLUT4 distributes between recycling endosomes and the insulin-responsive compartment. A handful of proteins that bind to GLUT4 appear to regulate its half-life (e.g. Ubc9) and tethering within endomembranes (e.g. TUG). Insulin-derived signals promote not only GLUT4 mobilization toward the PM but also its traffic between endosomal compartments and internalization from the PM. Class IA phosphatidylinositol (PI) 3-kinase plays a pivotal role at several steps of GLUT4 mobilization. The PI 3-kinase --> atypical PKC and --> Akt/PKB --> AS160 signaling cascades are major regulators of GLUT4 exocytosis aided by small GTPases. At the cell periphery, GLUT4-containing vesicles tether, dock, and fuse with the PM assisted by the exocyst complex followed by engagement of a soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex [with vesicle-associated membrane protein (VAMP)2 as the vesicular (v)-SNARE and soluble NSF-attachment protein (SNAP)23 and syntaxin4 as target (t)-SNAREs] regulated by the accessory proteins Munc18c, Synip and Tomosyn. Vesicle tethering and fusion are regulated by insulin through input from class IA PI 3-kinase.
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Some GLUTs are insulin-dependent transporters, such as GLUT4 in skeletal muscle.
“Moreover, some of these GLUTs are insulin-dependent transporters such as GLUT4 in skeletal muscle [30,31], which may facilitate glucose and 18 F-FDG cell uptake in patients with high insulin level, and may result in diminishing glucose and 18 F-FDG cell uptake in insulin resistance status.”
The prominent type of muscle glucose transporter is GLUT4, which is insulin-dependent, in contrast to tumors, which mainly overexpress Glut-1 and Glut-3 transporters that are not insulin-sensitive.
“The prominent type of muscle glucose transporter is GLUT4, which is insulin-dependent [30,31,93], in contrast to tumors which mainly overexpress Glut-1 and Glut-3 transporters, which are not insulin-sensitive [27,29,94].”
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Improved insulin sensitivity after exercise: focus on insulin signaling
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Insulin does not regulate glucose transport and metabolism in human endothelium
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Intrapatient variability of 18F-FDG uptake in normal tissues
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- Authors
- Ishiki, M., & Klip, A.
- Affiliations
- Hospital for Sick Children (CA)
- Corresponding author
- Klip, Amira
- ORCID
- Klip, Amira
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2005-12
- Volume
- 146
- Issue
- 12
- Pages
- 5071-5078
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2097079712
- Cited by
- 281
- References
- 90
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 6 · 2023: 9 · 2022: 3 · 2021: 4 · 2020: 9 · 2019: 2 · 2018: 7 · 2017: 6 · 2016: 8 · 2015: 11 · 2014: 8 · 2013: 16 · 2012: 17
- FWCI
- 13.42
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Diabetes Association
- Canadian Institutes of Health Research
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Keywords
- GLUT4, glucose transporter trafficking, insulin signaling, GGA2, EHD1, microtubules, recycling endosomes, Ubc9, tugboats, PI3K/Akt signaling, atypical PKC, AS160, small GTPases, exocyst complex, SNARE complex, Munc18c, tomosyn, adipocytes, muscle cells
- MeSH terms
- Animals, Tissue Distribution, Signal Transduction, Protein Transport, Glucose Transporter Type 4
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