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9560 rockville pike, bethesda, MD 20814-3991
 

 


Hepcidin Regulation of Iron Transport
Sponsored by APS Gastrointestinal and Liver Physiology Section and The American Society of Nutrition
Channels and Transporters Track

Sunday, April 6 — 10:30 AM-12:30 PM
San Diego Convention Center — Room 28 C/D
 
Chaired:

Marianne Wessling-Resnick, Harvard Sch. of Pub. Hlth.
James Collins, SUNY Buffalo
Mitch Knutson, Univ. of Florida

Since the discovery of hepcidin’s role in iron metabolism in 2001 [Pigeon et al., JBC 276: 7811] and the subsequent finding in 2004 that it functions as a ligand to induce degradation of the iron exporter ferroportin [Nemeth et al. Science 306: 2090], there has been an explosion of literature on this peptide hormone and its control of iron homeostasis. Imbalances in hepcidin gene expression are linked to genetic disorders of iron loading (hemochromatosis) and upregulation of the peptide is implicated in the anemia of chronic disease (ACD).  Moreover, it is tightly linked to inflammatory responses that contribute to “nutritional immunity”. Due to its apparent function in regulation of the basolateral iron transport machinery in the gut, it is important that the GI community be kept abreast of the function of this iron regulatory hormone and its implicated role in disease states.  One critical aspect is the development of new assays to detect circulating levels of the peptide.  A second important and emerging area is the elucidation of signal transduction pathways that modulate hepcidin gene expression in the liver.

Learning Objectives:  To present an overview of the role of hepcidin in iron homeostasis; to consider the metabolic regulation of hepcidin gene expression; and to define the best possible clinical approaches to determine circulating hepcidin levels.