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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
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| 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.
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