The role of hepcidin in iron metabolism in athletes

Abstract

Hepcidin is a peptide that was discovered in 2000, it is synthesized in the liver and it goes into circulation. There are three forms of hepcidin, hepcidin-25, hepcidin-22 and hepcidin-20. The first form is the most studied and its role is the most significant. Hepcidin-25 is considered to be a major regulator of the absorption of dietary iron as well as its release from cells. It achieves its regulatory function by preventing the function of ferroportin, the major cellular iron exporter. Ferroportin is a protein whose function is to release iron from the cells on which it is located (macrophages, hepatocytes and enterocytes). Hepcidin-25 induces degradation of ferroportin, resulting in an increase in intracellular iron stores. It also reduces the absorption of iron from food and thus reduces the concentration of circulating iron. During physical activity, the concentration of hepcidin increases at an intensity of 65% VO2 max, and maximum values are reached at 90-95% VO2 max. Not only intensity, but also the volume of physical activity influence its concentration. Studies showed that hepcidin expression during physical activity is influenced by inflammation, iron status, erythropoiesis and hypoxia. It is considered one of the causes of anemia in athletes. There are potential methods for neutralizing hepcidin (monoclonal antibodies and antagonists) and reducing its expression (erythropoietin doping, which is forbidden in sport, anti-IL-6 antibodies, STAT and BMP modulators). Given its important role in iron metabolism, which is essential for the transport of oxygen in the body, it can affect sports performance. It is still the subject of many research.