Iron Absorption
The mechanism of iron absorption has proceeded in two
stages. When they enter the cells of the mucosa, the Fe2+ ions are bound to
transport
substances like DCT1 (Divalent Cation Transporter). Before
entering into the blood plasma, they are oxidized to Fe3+ by endo-oxidase I
(ceruloplasmin) and bound in this form to transferrin.
Iron is absorbed as Fe2+ in the duodenum and in the upper jejunum. Since iron in food occurs predominantly in the trivalent form it must (apart from the heme-bound Fe2+ component) first be reduced, e.g. by ascorbic acid (vitamin C).
To learn more about Iron absorption watch below video.
This explains why only about 10% of the iron in food, corresponding to about 1 mg Per day, is generally absorbed. The average daily iron intake from foods and supplements is 13.7–15.1 mg/day in children aged 2–11 years, 16.3 mg/day in children and teens aged 12–19 years, and 19.3–20.5 mg/day in men and 17.0–18.9 mg/day in women older than 19. The median dietary iron intake in pregnant women is 14.7 mg/day.
The actual iron uptake fluctuates considerably, depending on absorption-inhibiting and absorption-promoting influences in the upper part of the small intestine.
Iron absorption is predominantly regulated at the basolateral surface of the duodenal enterocyte by control of iron export through ferroportin into plasma.
Iron is taken up into the duodenal enterocyte on the apical membrane via DMT1 and is stored or exported during its life span of a few days. If iron retained within the enterocyte is no exported, it will be lost as duodenal enterocytes are shed in the gastrointestinal tract.
Factors that Increase and Decrease Iron Absorption
Food Enhancing Iron Absorption:
- Almost all foods containing Vitamin C
- Citrus fruits like lemon, orange
- Amla, Tomatoes
Foods Reducing Iron Absorption:
- Calcium containing food
- Milk
- Curd
- Cheese
- Food containing high fiber
- Foods rich in phytates
- Legumes
- Grains
- Tea
- Coffee
The human body’s rate of iron absorption appears to respond
to a variety of interdependent factors, including total iron stores, the extent
to which the bone marrow is producing new red blood cells, the concentration of
hemoglobin in the blood, and the oxygen content of the blood. The body also
absorbs less iron during times of inflammation, in order to deprive bacteria of
iron. Recent discoveries demonstrate that hepcidin regulation of ferroportin is
responsible for the syndrome of anemia of chronic disease.
Ferroportin is also expressed on macrophages. As a consequence of their involvement in erythrophagocytosis of senescent RBCs, macrophages break down hemoglobin and recycle iron. Kupffer cells, residing in the liver sinusoids, and red pulp macrophages in the spleen are the major populations of macrophages responsible for steady-state erythrophagocytosis. As in duodenal enterocytes, iron liberated from hemoglobin is either exported via ferroportin or sequestered within cytosolic ferritin.