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ARS Home » Southeast Area » New Orleans, Louisiana » Southern Regional Research Center » Food Processing and Sensory Quality Research » Research » Publications at this Location » Publication #264448
Title: Rethinking iron regulation and assessment in iron deficiency, the anemia of chronic disease, and obesity: introducing Hepcidin

Author
item Tussing Humphreys, Lisa
item PUSATCIOGLU, CENK - University Of Illinois
item NEMETH, ELIZABETA - University Of California
item BRAUNSCHWEIG, CAROL - University Of Illinois

Submitted to: Journal Of The American Dietetic Association
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/17/2011
Publication Date: 3/1/2012
Citation: Tussing Humphreys, L.M., Pusatcioglu, C., Nemeth, E., Braunschweig, C.L. 2012. Rethinking iron regulation and assessment in iron deficiency, the anemia of chronic disease, and obesity: introducing Hepcidin. Journal Of The American Dietetic Association. 112(3):391-400.

Interpretive Summary: Iron is an important nutrient throughout all stages of human life. Iron is tightly regulated in the body because it can be toxic, and humans are unable to get rid of large amounts. An important protein was recently discovered that controls iron movement from both the diet and from storage sites within the body, which is called hepcidin. Hepcidin controls the channel in which iron enters into our system. High levels of hepcidin turn off this iron channel, and can prevent dietary iron and stored iron from entering circulation. Low iron intake from the diet, chronic, inflammatory diseases, and obesity are associated with negative changes in iron status in both adults and children. Research has indicated that hepcidin is elevated in chronic and inflammatory diseases, as well as obesity, and may be the reason iron status is altered in these conditions. This high level of hepcidin observed in chronic and inflammatory diseases and obesity may prevent dietary iron supplementation from being effective. Understanding the biological processes responsible for changes in iron status, and appropriately assessing iron status using traditional and nontraditional clinical tests, is important in determining the most appropriate therapy.

Technical Abstract: Adequate iron availability is essential to human development and overall health. Iron is a key component of oxygen-carrying proteins; a vital player in cellular metabolism, and essential to cell growth and differentiation. Tight regulation of iron at the systemic and cytosolic level is necessary because iron is highly toxic, and humans are unable to excrete large amounts. Hepcidin, a small peptide hormone produced mainly by the liver, acts as the key regulator of systemic iron homeostasis. Hepcidin controls movement of iron into plasma by diminishing the activity of the sole known iron exporter ferroportin-1 (Fpn). Down-regulation of the Fpn exporter results in sequestration of iron within intestinal enterocytes, hepatocytes, and iron storing macrophages, reducing iron bioavailability. Hepcidin is increased by higher circulating body iron levels and a pro-inflammatory state. Erythropoiesis and low circulating iron levels are associated with decreased hepcidin expression. Inadequate dietary iron intake, chronic and acute inflammatory conditions, and obesity are each associated with alterations in iron homeostasis and anemia in children and adults. Recent studies indicate that both the anemia of chronic disease and obesity are associated with increased hepcidin, suggesting dietary repletion may not be effective. The recent discovery of hepcidin, coupled with the proper selection of traditional and novel clinical markers of iron status, can allow practitioners to better understand the etiology of iron dysregulation within the context of iron deficiency, the anemia of chronic disease and obesity, and determine the most appropriate therapy.