Iron absorption in the duodenum is regulated by hepcidin, secreted by the liver. In iron-deficiency anaemia, serum hepcidin is LOW. The consequence of low hepcidin on intestinal iron absorption is:

• A Reduced ferroportin expression, decreasing iron export from enterocytes into blood
• B Reduced DMT-1 (divalent metal transporter 1) expression, decreasing iron uptake from the lumen
• C Increased ferroportin activity on basolateral enterocyte surface, allowing more iron to enter the portal circulation ✓
• D Increased hephaestin activity, reducing Fe3+ to Fe2+ in the duodenal lumen

Explanation

Hepcidin binds to ferroportin (the only known iron export channel, on basolateral enterocyte surface and macrophages) and causes its internalization and degradation. When iron stores are adequate, liver hepcidin is high → ferroportin is degraded → iron is trapped in enterocytes and shed with them → less iron enters blood. In iron deficiency, hepcidin is suppressed → ferroportin is abundant on basolateral surface → iron absorbed from lumen via apical DMT-1 is efficiently exported into portal blood → increased net iron absorption.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.