This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for 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. 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. Female high performance varsity athletes will be studied at two time points approximately 3-6 months apart: pre-competitive season and at the peak of their competitive season, depending on the nature of each subject's sport. Laboratory values for the following parameters will be obtained: hepcidin, iron, ferritin, transferrin/transferrin saturation, and interleukin-6. The study design will be before-after. Data will be analyzed via the Pearson product moment correlation or the Spearman rank correlation to detect correlations between the primary outcome variables hepcidin and ferritin and the remainder of the variables.
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