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Which receptor (transporter) helps in improvement of insulin resistance in DM2 (type 2 diabetes mellitus) with regular exercise and physical activity?
Which receptor (transporter) helps in improvement of insulin resistance in DM2 (type 2 diabetes mellitus) with regular exercise and physical activity?
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Which GLUT is insulin-responsive in skeletal muscle and also recruited to the membrane by muscle contraction (via AMPK/Ca²⁺)?
Updated On: Jun 22, 2026
- GLUT1
- GLUT4
- GLUT2
- GLUT3
Show Solution
The Correct Option is B
Solution and Explanation
The key is to remember the one glucose transporter that responds both to insulin and to muscle contraction - GLUT4.
Skeletal muscle is the largest site of insulin-stimulated glucose disposal, and it does this through GLUT4, which sits in intracellular vesicles and moves to the cell surface only when triggered. In type 2 diabetes, insulin's ability to trigger that translocation is blunted (insulin resistance), so glucose stays in the blood.
Exercise provides a second, parallel trigger for GLUT4 that bypasses the faulty insulin pathway. Contracting muscle raises intracellular $Ca^{2+}$ and activates AMP-activated protein kinase (AMPK); both independently drive GLUT4 vesicles to the membrane. With regular training, muscle also up-regulates total GLUT4 content and improves insulin sensitivity of the transporter. The net effect is greater glucose clearance into muscle and reduced insulin resistance - the clinically observed benefit of physical activity in DM2.
By contrast, GLUT1 handles constant baseline uptake (red cells, brain barrier), GLUT2 is the high-capacity sensor of liver/$\beta$-cells and gut, and GLUT3 supplies neurons - none are the exercise-recruited muscle transporter.
Therefore the answer is GLUT4 (option B).
Skeletal muscle is the largest site of insulin-stimulated glucose disposal, and it does this through GLUT4, which sits in intracellular vesicles and moves to the cell surface only when triggered. In type 2 diabetes, insulin's ability to trigger that translocation is blunted (insulin resistance), so glucose stays in the blood.
Exercise provides a second, parallel trigger for GLUT4 that bypasses the faulty insulin pathway. Contracting muscle raises intracellular $Ca^{2+}$ and activates AMP-activated protein kinase (AMPK); both independently drive GLUT4 vesicles to the membrane. With regular training, muscle also up-regulates total GLUT4 content and improves insulin sensitivity of the transporter. The net effect is greater glucose clearance into muscle and reduced insulin resistance - the clinically observed benefit of physical activity in DM2.
By contrast, GLUT1 handles constant baseline uptake (red cells, brain barrier), GLUT2 is the high-capacity sensor of liver/$\beta$-cells and gut, and GLUT3 supplies neurons - none are the exercise-recruited muscle transporter.
Therefore the answer is GLUT4 (option B).
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