Question

Hepcidin inhibits which of the following?

• A. Absorption of cobalamin
• B. Transfer of iron into enterocytes
• C. Folic acid synthesis
• D. Respiratory oxidase

Hint:

Think of the liver hormone that shuts down ferroportin during inflammation.

Answer 1

The Correct Option is B

Mnemonic angle: remember hepcidin as the iron gatekeeper that locks the exit door. The exit door is ferroportin, the channel that ships iron from gut cells and macrophages into blood. When hepcidin is high (as in chronic inflammation), it degrades ferroportin, and iron gets trapped inside the enterocyte. Trapped iron is then lost when the cell sloughs off, so net absorption falls. That makes transfer of iron into enterocytes the step hepcidin blocks, and is why anemia of chronic disease shows low serum iron despite full stores. Quick elimination of the rest: cobalamin uptake is an intrinsic-factor and ileal-receptor job, folic acid synthesis is something only bacteria do (a drug target, not a hepcidin one), and respiratory oxidase sits in mitochondrial energy production. None touch iron transport. So option (b) is the only fit. Diet pearl to recall alongside: vitamin C keeps iron in the absorbable ferrous form and boosts uptake, whereas tea tannins bind iron and reduce it.