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Regulation of hepcidin expression at high altitude.

Abstract
Enhanced erythropoietic drive and iron deficiency both influence iron homeostasis through the suppression of the iron regulatory hormone hepcidin. Hypoxia also suppresses hepcidin through a mechanism that is unknown. We measured iron indices and plasma hepcidin levels in healthy volunteers during a 7-day sojourn to high altitude (4340 m above sea level), with and without prior intravenous iron loading. Without prior iron loading, a rapid reduction in plasma hepcidin was observed that was almost complete by the second day at altitude. This occurred before any index of iron availability had changed. Prior iron loading delayed the decrease in hepcidin until after the transferrin saturation, but not the ferritin concentration, had normalized. We conclude that hepcidin suppression by the hypoxia of high altitude is not driven by a reduction in iron stores.
AuthorsNick P Talbot, Samira Lakhal, Thomas G Smith, Catherine Privat, Annabel H Nickol, Maria Rivera-Ch, Fabiola León-Velarde, Keith L Dorrington, David R Mole, Peter A Robbins
JournalBlood (Blood) Vol. 119 Issue 3 Pg. 857-60 (Jan 19 2012) ISSN: 1528-0020 [Electronic] United States
PMID22130801 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antimicrobial Cationic Peptides
  • GDF15 protein, human
  • Growth Differentiation Factor 15
  • HAMP protein, human
  • Hepcidins
  • Iron, Dietary
  • Transferrin
  • Erythropoietin
  • Ferritins
  • Iron
Topics
  • Adult
  • Altitude
  • Antimicrobial Cationic Peptides (metabolism)
  • Case-Control Studies
  • Erythropoiesis (genetics, physiology)
  • Erythropoietin (metabolism)
  • Ferritins (metabolism)
  • Gene Expression Regulation
  • Growth Differentiation Factor 15 (metabolism)
  • Hepcidins
  • Homeostasis
  • Humans
  • Hypoxia (complications, metabolism)
  • Iron (metabolism)
  • Iron Metabolism Disorders (etiology, metabolism)
  • Iron, Dietary (metabolism)
  • Transferrin (genetics, metabolism)
  • beta-Thalassemia (metabolism)

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