Linking hypoxia and iron homeostasis: a 'plate' full of factors

Hepcidin, a 25-amino acid peptide expressed almost exclusively in the liver, is the central regulator of systemic body iron homeostasis. Since its initial identification and characterisation as an antimicrobial peptide, it has become clear that hepcidin plays a role in many metabolic processes. Mutations in hepcidin lead to one form of the severe iron overload disorder juvenile haemochromatosis (type 2B). Hepcidin is a negative regulator of iron absorption and recycling; under normal conditions, increased iron in the body results in an enhanced secretion of hepcidin by the liver, the central organ responsible for iron regulation. Hepcidin then binds the iron transporter ferroportin, inducing its internalisation and degradation, thus reducing iron absorption by enterocytes of the duodenum, and iron recycling by macrophages.1 Hepcidin itself is also regulated by other factors besides iron levels; these include hypoxia, erythropoietic activity, proinflammatory cytokines and other hormones.2 These factors thus...
Source: Gut - Category: Gastroenterology Authors: Tags: Commentary Source Type: research