In adipose and skeletal muscle cells, insulin stimulates:
1) active transport of glucose
2) opening of chemically-gated channels
3) entry of insulin into cells
4) opening of glucose channels
5) increased cell membrane glucose carriers
The correct answer and explanation is:
Correct Answer:
5) increased cell membrane glucose carriers
Explanation (300 words):
Insulin plays a critical role in regulating blood glucose levels, especially after meals. In adipose (fat) and skeletal muscle cells, insulin promotes glucose uptake primarily by increasing the number of glucose transport proteins on the cell membrane.
These glucose transport proteins are known as GLUT4 transporters. Normally, GLUT4 resides inside the cell, stored in vesicles. When insulin binds to its receptor on the surface of adipose or muscle cells, it triggers a signal transduction pathway that causes these vesicles to move to the cell membrane and fuse with it. This process increases the number of glucose carriers (GLUT4 proteins) on the membrane, making it easier for glucose to enter the cell from the bloodstream.
The mechanism is not about:
- (1) Active transport of glucose – Glucose entry is through facilitated diffusion, not active transport.
- (2) Opening of chemically-gated channels – These are typical for ions like Na⁺ or K⁺, not glucose.
- (3) Entry of insulin into cells – Insulin binds to surface receptors; it does not enter the cell to function.
- (4) Opening of glucose channels – GLUT4 is a carrier protein, not a channel that opens like an ion channel.
Thus, insulin does not open a “channel” but rather increases the number of GLUT4 carriers, which work via facilitated diffusion, a passive process that depends on glucose concentration gradients.
This effect is essential in lowering blood glucose levels after meals and providing muscle and fat cells with glucose for energy production or fat synthesis. A failure in this mechanism, such as in Type 2 diabetes, results in poor glucose uptake despite normal or high insulin levels, often due to insulin resistance where cells fail to respond properly to insulin.