Absorption of Dietary Iron
Iron absorption occurs primarily in the duodenum and proximal jejunum. Because the human body lacks a physiological pathway for active iron excretion, absorption is strictly regulated to maintain homeostasis.
Forms of Dietary Iron
Dietary iron exists in two distinct forms, which are absorbed through different mechanisms:
| Feature | Heme Iron | Non-Heme Iron |
|---|---|---|
| Source | Animal products (Hemoglobin/Myoglobin) | Plants, fortified foods, dairy |
| Bioavailability | High (15-35%) | Low (2-20%) |
| Absorption Path | Heme Carrier Protein 1 (HCP1) | Divalent Metal Transporter 1 (DMT1) |
The Mechanism of Absorption
The Step-by-Step Pathway:
- Reduction: Ferric iron (Fe3+) from plants must be reduced to Ferrous iron (Fe2+) by the enzyme Duodenal Cytochrome B (DcytB) at the brush border.
- Uptake: Fe2+ is transported into the enterocyte via DMT1.
- Intracellular Fate: Once inside, iron is either stored as Ferritin (and lost when the cell sloughs off) or exported to the blood.
- Export: Iron exits the basal side of the cell via the only known iron exporter, Ferroportin.
- Oxidation: To be carried in the blood, iron must be converted back to Fe3+ by Hephaestin so it can bind to Transferrin.
Factors Influencing Absorption
- Enhancers: Vitamin C (Ascorbic acid) reduces Fe3+ to Fe2+, making it more soluble. Meat proteins also enhance uptake.
- Inhibitors: Phytates (grains), Polyphenols (tea/coffee), Calcium, and Oxalates bind iron and prevent its absorption.
Regulation by Hepcidin
Hepcidin is the "Master Regulator" hormone produced by the liver.
- When iron stores are high: Hepcidin levels rise and bind to Ferroportin, causing it to be internalized and degraded. This "locks" iron inside the enterocytes, preventing it from entering the blood.
- When iron stores are low: Hepcidin production is suppressed, allowing Ferroportin to remain active on the cell surface for maximum iron export.