Journal
BLOOD
Volume 117, Issue 10, Pages 2953-2959Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2010-08-299859
Keywords
-
Categories
Funding
- Boehringer Ingelheim, Germany
- Banca Intesa San Paolo, Italy
- A. DeMari
- CutAway srl
- Sport Specialist
- EuroTech
- Moccagatta Pogliani Associati
- DiaTecne
- FMS
- GE Healthcare
- InterCure
- Microlife
- Omron
- Oridion
- Pollution
- Rotem
- Sapio life
- Seda SpA
- SensorMedics
- Spacelabs Healthcare
- srLabs
- Tecnoel srl
- TensioMed
- Webbit srl companies
- Cariplo Foundation [2009-2483]
- Ministry of Instruction, University and Research [PRIN 2008N73CJ5-004]
Ask authors/readers for more resources
Iron is tightly connected to oxygen homeostasis and erythropoiesis. Our aim was to better understand how hypoxia regulates iron acquisition for erythropoiesis in humans, a topic relevant to common hypoxia-related disorders. Forty-seven healthy volunteers participated in the HIGHCARE project. Blood samples were collected at sea level and after acute and chronic exposure to high altitude (3400-5400 m above sea level). We investigated the modifications in hematocrit, serum iron indices, erythropoietin, markers of erythropoietic activity, interleukin-6, and serum hepcidin. Hepcidin decreased within 40 hours after acute hypoxia exposure (P < .05) at 3400 m, reaching the lowest level at 5400 m (80% reduction). Erythropoietin significantly increased (P < .001) within 16 hours after hypoxia exposure followed by a marked erythropoietic response supported by the increased iron supply. Growth differentiation factor-15 progressively increased during the study period. Serum ferritin showed a very rapid decrease, suggesting the existence of hypoxia-dependent mechanism(s) regulating storage iron mobilization. The strong correlation between serum ferritin and hepcidin at each point during the study indicates that iron itself or the kinetics of iron use in response to hypoxia may signal hepcidin down-regulation. The combined and significant changes in other variables probably contribute to the suppression of hepcidin in this setting. (Blood. 2011;117(10):2953-2959)
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available