Iron is absorbed by the gut, used to synthesize hemoglobin and stored in liver cells. Learn the details of iron absorption, storage and metabolism.
Our body requires iron as it is a component of hemoglobin, the oxygen-carrying molecule present in red blood cells. The body gets its iron from dietary sources. Iron deficiency anemia is result of the body not getting enough iron to synthesize hemoglobin.
How does the body absorb iron from the food we eat? Can iron be stored in the body? How does the body lose iron? Answering these questions can help us understand, and therefore prevent, iron deficiency anemia.
Iron Absorption From the Small Intestine
Iron present in the food we eat is absorbed mainly by the small intestine, especially the duodenum. But the intestinal cells can’t just take up dietary iron. First of all, iron has to be present in the ferrous (Fe2+) rather than the ferric (Fe3+) form. Ferrous ions then have to bind with apotransferrin, a protein secreted by the liver into the intestines via bile. The combination of apotransferrin with iron is now called transferrin.
Transferrin first binds to receptors on the surface of intestinal cells. It is then absorbed into the cell and later enters blood circulation through the rich network of blood capillaries present close to the intestinal cells.
One important fact about iron uptake is that very little iron is actually absorbed from our diet. That is, if a meal contains about 10 to 20 mg of iron, only 1 mg is absorbed. Also, while some substances like phytates hinder iron absorption, others like vitamin C enhance it. This is why many iron supplements incorporate vitamin C.
Iron Storage and Metabolism – Ferritin and Hemosiderin
Most of the iron in the body is utilized in hemoglobin synthesis. Iron is also present in myoglobin in muscles, cytochromes and enzymes like cytochrome oxidase, peroxidase and catalase. Transferrin circulates in the blood stream carrying with it the iron absorbed in the intestines, ready to deposit it wherever required. While about 65% of the body’s iron is in hemoglobin, about 15 to 30% is in the storage form.
Excess iron is mainly stored in hepatocytes or liver cells and to a smaller extent in bone marrow cells. In these cells, iron is taken up by a large protein molecule called apoferritin to form ferritin. Ferritin is the storage form of iron and may contain either small or large quantities of iron. Iron in excess of this is stored as hemosiderin, another less-soluble storage form.
Whenever the level of iron in plasma dips, iron stored in ferritin is released, to circulate as transferrin and available for utilization anywhere in the body. In the bone marrow, transferrin is engulfed by erythroblasts, precursor cells of RBCs, for the synthesis of hemoglobin. So even protein deficiency, where there is decreased transferrin with failure to deliver iron to the erythroblasts, can result in anemia.
RBCs typically have a life span of about 120 days. When they are destroyed, their hemoglobin content is released into circulation to be consumed by scavenger cells called macrophages. Iron from hemoglobin is once again released into circulation to be taken up by transferrin. About 0.6mg iron is excreted in feces each day. More iron is lost in hemorrhage or bleeding, as during menstruation.
Regulation of Iron Absorption
Iron absorption is regulated by a feedback mechanism. As excess iron completely binds to all the ferritin in the body, even transferring becomes saturated with iron and as a result intestinal absorption of iron becomes greatly reduced or ceases completely. In such a state, even the liver reduces its production of apotransferrin. But sometimes massive iron absorption can occur overriding these mechanisms and result in excessive hemosiderin deposition.
Iron is absorbed by cells of the small intestine from the food we eat. While most of it is used for hemoglobin synthesis, excess iron is stored in the form of ferritin. Studying iron metabolism helps prevent and treat iron deficiency anemia.