Nutrition is medicine: dietary inhibition of hepcidin expression.Comments Comment on: Br J Nutr. 2014 Apr 14;111(7):1181-9; PMID: 24387766

摘要

Poor Fe status, often characterised as Fe de?ciency (ID, poor Fe stores) and Fe-de?ciency anaemia (IDA, ID with diminished Hb), affects billions of people in both the developing and developed world (1,2) . Poor Fe status affects both physical and neuropsychological performance, and has profound effects on work performance and productivity (3) . Historically, efforts to treat and prevent ID and IDA have included the provision of added Fe to the diet in the form of forti?cation and supplementation, and recent systematic reviews have indicated that these countermeasures appear to be somewhat effective in restoring Fe status (4,5) . However, the discovery of hepcidin, often described as the central regulator of Fe homeostasis, may provide a new target for the treatment and prevention of ID and IDA. Hepcidin regulates Fe status primarily through its effects on Fe export from the enterocyte, macrophage and hepatocyte, where it binds and degrades ferroportin 1, the export protein responsible for cellular Fe egress (6) .