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Updated: Jun 10, 2026
08:01
Measurement of Insulin- and Contraction-Stimulated Glucose Uptake in Isolated and Incubated Mature Skeletal Muscle from Mice
Published on: May 16, 2021
Muscling in on GLUT4 kinetics.
Communicative & Integrative Biology
|August 18, 2010
Summary
Insulin stimulates glucose transporter GLUT4 to move to the cell surface in muscle and fat cells. However, L6 muscle cells achieve this via reduced GLUT4 removal, unlike fat cells.
Area of Science:
- Cell biology
- Metabolism
- Molecular biology
Background:
- Insulin stimulates glucose uptake by moving glucose transporter GLUT4 to the plasma membrane (PM).
- In adipocytes, this involves increasing GLUT4 in the endosomal recycling system and exocytosis rate.
- GLUT4 translocation to the PM is crucial for maintaining glucose homeostasis.
Purpose of the Study:
- To investigate the kinetic mechanisms regulating GLUT4 translocation in L6 skeletal muscle cells.
- To compare GLUT4 regulation in L6 cells with that in adipocytes.
Main Methods:
- Kinetic analysis of GLUT4 translocation in L6 skeletal muscle cells.
- Investigated the effects of insulin and AMPK agonists on GLUT4 trafficking.
Main Results:
- Insulin increased cell surface GLUT4 in L6 cells, similar to adipocytes.
- However, the mechanism differed: insulin primarily reduced the GLUT4 endocytosis rate constant in L6 cells.
- AMPK agonists showed similar effects, reducing the endocytosis rate constant.
Conclusions:
- L6 skeletal muscle cells utilize a distinct mechanism for insulin-stimulated GLUT4 translocation compared to adipocytes.
- This highlights that different cell types can achieve the same biological outcome through varied molecular pathways.
- The findings emphasize the cell-specific regulation of glucose transport.
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