Step 1: Hepcidin is the master regulatory hormone of iron metabolism, made mainly in the liver. It controls how much iron enters the blood.
Step 2: Hepcidin binds the iron exporter ferroportin on enterocytes and macrophages and triggers its degradation. With ferroportin gone, iron cannot be moved out of the enterocyte into the circulation, so effective iron absorption drops. This is why option (b), transfer of iron into enterocytes, is the action it blocks.
Step 3: The other options are unrelated. Cobalamin absorption needs intrinsic factor, folic acid synthesis is a bacterial pathway, and respiratory oxidase belongs to the electron transport chain. None are hepcidin targets.
Clinical link: Vitamin C reduces ferric to ferrous iron and forms soluble complexes that aid absorption, while tannins in tea form insoluble complexes that lower it.
Ref: Harper's Illustrated Biochemistry, 31e, Iron Metabolism.