Iron absorption in the duodenum from non-haem dietary sources requires reduction of Fe³⁺ to Fe²⁺. This reduction is catalysed by duodenal cytochrome b (DcytB) on the apical membrane of enterocytes. The subsequent transporter that imports Fe²⁺ into the enterocyte and is also the transporter mutated in DMT1-deficiency anaemia is:
- A DMT1 (divalent metal transporter 1, also called SLC11A2) ✓
- B Ferroportin (SLC40A1) on the basolateral membrane
- C Transferrin receptor 1 (TfR1) on the apical membrane
- D Hephaestin coupled with caeruloplasmin
Explanation
Non-haem iron absorption requires: gastric acid and ascorbate reducing Fe³⁺ → Fe²⁺, apical DcytB further reducing Fe³⁺, and DMT1 (SLC11A2) cotransporting Fe²⁺ with H⁺ across the apical membrane into the enterocyte cytoplasm. Inside the cell, iron is stored as ferritin or transferred to basolateral ferroportin for export into the portal circulation. Ferroportin is the sole known cellular iron exporter; hepcidin (from the liver) internalises ferroportin, explaining why iron absorption decreases in inflammatory states. TfR1 mediates endocytosis of transferrin-bound iron in non-enterocyte cells.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.