Nutrition and the Developing Brain by Victoria Hall Moran & Nicola M. Lowe

Author:Victoria Hall Moran & Nicola M. Lowe
Language: eng
Format: epub
Publisher: CRC Press

6.2.5 PHYSIOLOGY OF IRON HOMEOSTASIS

With a large amount of iron associated with red blood cells, the natural turnover of erythrocytes results in substantial quantities of iron (~20 mg/day) cycling into and out of haemoglobin. This is much less than the amounts of iron absorbed from the diet (~1 mg/day in adults). There is no specific mechanism to excrete excess iron in humans and, although there is some evidence for loss through excretion across the gut, overall iron status is maintained by regulating absorption.

Iron is largely absorbed in the duodenum and jejunum. Very little iron is absorbed in the lower intestine or colon, and iron in the colon may, in fact, be harmful, since it has the capacity to go through redox cycling, with risk of damage to colon cells. Haem iron is more bioavailable than non-haem iron, but in normal diets, non-haem iron is present in much higher amounts (up to about 90%). Additionally, there are components in the diet that can increase or decrease bioavailability. Phytate, for example, can bind iron and reduce its absorption, while vitamin C will increase absorption by reducing Fe3+ to Fe2+, which is the form taken up by the enterocyte. Additionally, meat contains factors that stimulate absorption, possibly by increasing the solubility of the iron.

The liver is the major regulator of whole-body iron status, coordinating an elaborate system to store surplus iron to make it available when it is needed and also to regulate uptake from the gut (Linder 2013). The liver stores iron safely in ferritin. The ferritin apo-protein consists of approximately 20 monomers which combine to form a hollow shell, within which the iron is stored. Some of the ferritin finds its way into serum and circulating levels can be used to estimate liver iron stores with a reasonable degree of accuracy. When ferritin stores are adequate, the liver produces a small peptide, hepcidin, which enters the circulation and binds to ferroportin, the protein regulating iron efflux from the gut. The ferroportin becomes ubiquitinated and is degraded by the proteasome in the gut, reducing iron efflux from the cell as shown in Figure 6.1. Hepcidin also acts on macrophages to reduce the production of iron from the destruction of outdated erythrocytes. Hepcidin itself is regulated by many different factors (Figure 6.2) which unfortunately means that it cannot be used as a biomarker of iron status.

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