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How the body get rich source of iron

How the body get rich source of iron: Total body iron in healthy adults normally ranges between 3.50 grammes and 5.00 grammes and it is mostly stored within the liver, red blood cells, macrophages, bone marrow and muscles. However, low amount of iron is found in the kidney and brain. Iron is acquired via dietary intake and absorption of ferrous and heme iron by the intestinal cells. There is no dedicated way of excreting iron in the body, thus, most of the iron is recycled within the body from old red blood cells within the spleen and bone marrow and the remainder is stored in proteins such as ferritin/hemosiderin.

The iron cycling system involves four different cells: intestinal cells, blood cells, macrophages, and liver cells. Iron uptake starts at the intestinal cells membrane, which takes up ferrous iron and import this via the liquid solution of the cells through a metal ion transporter-1. The intestinal cells absorb haeme which makes up the red blood cells via the heme carrier protein-1. The ferrous iron in the liquid part of the within the intestinal cells can be stored as ferritin, or exported through the protein known as ferroportin at the basal membrane site. This ferroportin exports iron into fluids. Thus allowing the iron transport protein transferrin to bind two iron. Transferrin is taken up by bone marrow cells which bind two transferrin proteins. In the bone marrow cells, the iron is released and enters the powerhouse for heme synthesis to produce haemoglobin. The recovery of iron from haemoglobin involves recycling of damaged red blood cells via the spleen macrophages.

How the body get rich source of iron
How the body get rich source of iron: Iron is acquired via dietary intake and absorption of ferrous and heme iron by the intestinal cells. Adapted from Koury et al 2015

Liver cells are also able to assess transferrin. Under high levels of transferrin, liver cells increase synthesis and release of the protein called hepcidin which indirectly reduce iron absorption from intestinal cells and reduce iron release from macrophages. When iron is low the hepcidin is reduced to allow more iron uptake. Any problem with this process could lead to disease condition such as  saturation hemochromatosis type 1 and type 3.

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