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A new study from Department of Physiology, Anatomy & Genetics has addressed a long-standing gap in our understanding of systemic iron homeostasis. It provides the first formal demonstration that the hormone hepcidin controls iron reabsorption in the kidney, in a manner that impacts the body’s iron levels, under normal physiological conditions. It also demonstrates for the first time how this mechanism becomes critically important in the development of iron disorders.

Illustration showing iron reabsorption
In addition to absorption in the gut and recycling in the spleen, iron is also obtained through reabsorption in the kidney

Iron levels in the body are largely controlled by activity in two key organs: the gut, where we absorb iron from our diet, and the spleen, where we recycle red blood cells. The hormone hepcidin controls the availability of iron in the blood stream by inhibiting the iron exporter ferroportin in the gut and spleen. It has long been speculated that a third organ could be involved: an abundance of ferroportin has been observed in the kidney, implicating it in the reabsorption of iron from urine back into the circulation. However, the extent to which the kidney contributes to the regulation of iron in the body has so far been little understood. We do not know how important the kidney iron reabsorption is, nor how it is regulated.

A new study from the Lakhal-Littleton Research Group (Department of Physiology, Anatomy & Genetics - DPAG) has formally demonstrated that the kidney indeed reabsorbs iron back into the blood stream using ferroportin. Their findings show that if ferroportin in the kidney is blocked, there is a reduction in the body’s iron levels, which is quickly corrected by a compensatory increase in gut iron absorption.  According to Associate Professor Samira Lakhal-Littleton: “This means that under normal physiological conditions, the kidney is a less important  source of iron than the gut and spleen.”

Read the full story on the DPAG website.

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