Iron Metabolism in Human Body

Abstract

Animal and plant sources have haem and non-haem forms of iron. These two forms of iron have variable absorbability in the small intestine. Haem iron is available in animal protein in the forms of haemoglobin and myoglobin. This form of iron is absorbed faster than non-haem iron from vegetarian diet.

Ascorbate, citrate and amino acids act as absorption promoters. Phytic acid, tannins, oxalates, carbonates, phosphates and soil eating retard iron absorption. Duodenal cytochrome b (DCTYB) is a characteristic ferric reductase enzyme of the human body. It is located on the brush border surface of enterocytes. It reduces Fe³⁺ iron into highly soluble Fe²⁺ iron. Ferrous iron is actively transported across the cell membrane of enterocytes. Absorption of haem iron absorption is mediated by haem receptors. These are located on the microvilli of epithelial cells in the small intestine. Iron from the inside of mucosal cells can be exported to plasma by basolateral iron exporter proteins. Ferroportin-1 serves as the chief iron exporter from mucosal cells and hepatocytes. Hepcidin prevents the export of iron in circulation in condition of chronic inflammation like kidney failure and cirrhosis (Ashby et al. 2009). Iron deficiency during 0–3 years of life alters the morphology, physiology and bioenergetics of CNS. Iron is an essential cofactor in the process of myelination. Additional hypothesis related with the effect of iron deficiency on the neurodevelopment is the altered brain bioenergetics. Children who were iron deficient in infancy had comparatively poor physical activity and poor ability to verbalization at the age of 5 years irrespective of the iron supplements which corrected their iron deficiency during infancy.