Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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.

Similar stories

Can humans hibernate?

Illuminating new TEDx Talk from Professor of Sleep Physiology Vladyslav Vyazovskiy

Athena Swan Gold Award success for Nuffield Department of Primary Care Health Sciences

The award reflects the Department’s commitment to representation, progression and success for all. It acknowledges the innovative policies and practices developed across the department and the detailed action plans for improvement.

RECOVERY trial team awarded MRC Impact Prize for Outstanding Team Impact

The Medical Research Council Prize Committee has awarded the RECOVERY trial team the MRC Impact Prize 2022 for Outstanding Team Impact.

Professor Sir Chris Whitty brings greater understanding of epidemics to Oxford

Chief Medical Officer of England Professor Sir Chris Whitty KCB FMedSci delivers the Sherrington Prize Lecture: Public Understanding of Science to an audience of Oxford staff and students.

Multiple Debilitating Pains – New global study shows the experience of Endometriosis is rooted in a person’s genetics

Researchers at the University of Oxford in collaboration with 25 teams across the world have published the largest study to date of the genetic basis of endometriosis.

Study shows delaying treatment for localised prostate cancer does not increase mortality risk

Active monitoring of prostate cancer has the same high survival rates after 15 years as radiotherapy or surgery, reports the largest study of its kind.