Iron is a trace element essential for many biological processes. Iron metabolism is controlled by the regulatory hormone hepcidin; levels of which are influenced by factors including inflammation, erythropoiesis and repleteness of iron stores. Around half of measurable diversity in between individual iron biomarkers appears to be influenced or caused by genetic factors.
We hypothesize that genetic variation in hepcidin gene pathways significantly modulates iron homeostasis. This in turn may affect:
i) Responses to oral iron supplementation
ii) Host-protective hypoferremia.
We have devised a ‘Genes-in-Action’ (GiA) experimental study design to examine the molecular mechanisms of iron metabolism underlying these processes.
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