This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Hepcidin is a recently discovered iron regulatory hormone produced by hepatocytes. It controls the level of extracellular iron by decreasing iron absorption in the duodenum and causing iron sequestration in macrophages. Hepcidin production is stimulated by inflammation, especially by release of the cytokine interleukin-6. Cytokines have been found to increase with intense exercise. Female athletes, particularly endurance athletes, are commonly observed to have low serum iron and ferritin levels in the absence of anemia (iron deficiency without anemia). Our hypothesis is that hepcidin is upregulated in athletes during the competitive season. We propose that hepcidin is a major contributor to the development of iron deficiency without anemia in athletes during a competitive season. We further propose that athletes at risk for frank iron deficiency anemia who are identified early in the season via low ferritin levels will benefit from iron supplementation before hepcidin is upregulated (i.e. at the beginning of the season). This would have implications for all high performance women athletes, as it would suggest the need to check a serum ferritin prior to entering the competitive season.
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