The sodium gradient used for secondary active transport of glucose into intestinal mucosal cells is maintained by which primary transport mechanism?

The sodium gradient used for secondary active transport of glucose into intestinal mucosal cells is maintained by which primary transport mechanism?

• A. Sodium-potassium ATPase exporting Na+ out of the cell
• B. GLUT2 transporter moving glucose
• C. Sodium channel leak
• D. Proton pump in mitochondria

Answer: (A)

Maintaining the sodium gradient across the intestinal mucosa is achieved by a primary active transport pump that uses ATP to move sodium out of the cell in exchange for potassium coming in. This action keeps intracellular sodium low, creating a strong driving force for sodium to enter from the intestinal lumen. The same sodium gradient then powers the secondary active transport of glucose into the cell via a sodium-glucose cotransporter, which brings glucose in as sodium moves down its gradient. Once inside, glucose exits toward the blood through a separate transporter like GLUT2. The pump is essential because, without actively exporting sodium, the gradient would collapse and glucose uptake by the sodium-dependent transporter would fail. The other options don’t establish or maintain this gradient: a passive glucose transporter like GLUT2 handles glucose movement but not the gradient itself, a sodium leak pathway would dissipate the gradient, and a mitochondrial proton pump is involved in ATP generation, not directly in maintaining the sodium gradient used for glucose transport.

Maintaining the sodium gradient across the intestinal mucosa is achieved by a primary active transport pump that uses ATP to move sodium out of the cell in exchange for potassium coming in. This action keeps intracellular sodium low, creating a strong driving force for sodium to enter from the intestinal lumen. The same sodium gradient then powers the secondary active transport of glucose into the cell via a sodium-glucose cotransporter, which brings glucose in as sodium moves down its gradient. Once inside, glucose exits toward the blood through a separate transporter like GLUT2. The pump is essential because, without actively exporting sodium, the gradient would collapse and glucose uptake by the sodium-dependent transporter would fail. The other options don’t establish or maintain this gradient: a passive glucose transporter like GLUT2 handles glucose movement but not the gradient itself, a sodium leak pathway would dissipate the gradient, and a mitochondrial proton pump is involved in ATP generation, not directly in maintaining the sodium gradient used for glucose transport.