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Building GLUT4 Vesicles: CHC22 Clathrin's Human Touch.
Gwyn W Gould1, Frances M Brodsky2, Nia J Bryant3
1Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, 161 Cathedral Street, Glasgow G4 0RE, UK.
Trends in Cell Biology
|July 5, 2020
Summary
Insulin-stimulated glucose transport relies on GLUT4 vesicle delivery, a process differing between humans and rodents due to species-specific proteins like CHC22. Understanding these differences is key for treating type 2 diabetes.
Area of Science:
- Cell Biology
- Molecular Biology
- Endocrinology
Background:
- Insulin stimulates glucose transport via GLUT4 transporter delivery to the cell membrane.
- This process is impaired in type 2 diabetes (T2DM).
- Rodent models are widely used, but species-specific differences in GLUT4 trafficking exist.
Purpose of the Study:
- To discuss species-specific distinctions in GLUT4 sorting and trafficking.
- To highlight the role of the human-specific clathrin isoform, CHC22, in GLUT4 traffic.
- To explore implications for cell biology and diseases like T2DM.
Main Methods:
- Comparative analysis of GLUT4 trafficking pathways across species.
- Review of recent studies investigating the function of CHC22.
- Discussion of protein complexes involved in GLUT4 sorting.
Main Results:
- Identified species-specific differences in GLUT4 trafficking, particularly the involvement of CHC22 in humans.
- CHC22 mediates novel routes for GLUT4 trafficking not observed in rodents.
- Different sorting-protein complexes are associated with these distinct trafficking pathways.
Conclusions:
- Evolutionary plasticity in GLUT4 traffic necessitates considering species-specific mechanisms.
- CHC22 plays a crucial role in human GLUT4 trafficking, offering new insights into cellular glucose uptake.
- Understanding these pathways may reveal new therapeutic targets for T2DM and other metabolic diseases.
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