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Iron-Siderophore and Tumorigenesis
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Sayantan Maitra, Dibyendu Dutta
Cancer cells make metabolically available iron not only by increasing iron influx and decreasing iron storage but also by decreasing the iron efflux. Systemic iron levels are closely monitored by ferroportin–hepcidin regulatory axis. Ferroportin is expressed on the cell surface of enterocytes, and its expression is regulated by the circulatory peptide hormone hepcidin [18]. When levels of iron in storage and circulation are high, hepcidin is induced in hepatocytes via a bone morphogenetic protein (BMP)-mediated pathway and is released into the circulation. On the basolateral side of enterocytes, hepcidin binds to ferroportin and induces internalization of ferroportin into clathrin-coated pits and its subsequent lysosomal degradation (Figure 17.2), thus blocking the delivery of iron from the digestive tract to the blood [19,20].
Serum iron availability, but not iron stores, is lower in naturally menstruating than in oral contraceptive athletes
Published in European Journal of Sport Science, 2023
Víctor M. Alfaro-Magallanes, Nuria Romero-Parra, Laura Barba-Moreno, Beatriz Rael, Pedro J. Benito, Ángel E. Díaz, Rocío Cupeiro, Ana B. Peinado
Iron deficiency (ID) is one of the most prevalent nutrient deficiency worldwide and it is the predominant cause of anaemia among the 1.93 billion anaemic people globally (Ning & Zeller, 2019). Premenopausal women are one of the most affected population by ID and ID anaemia (IDA), with previous research suggesting athletes are those with the highest incidence of these conditions (Ning & Zeller, 2019; Sim et al., 2019). Iron is a key mineral in the human body involved in several physiological mechanisms at both the cellular and systemic level (Muckenthaler, Rivella, Hentze, & Galy, 2017), and which regulation is orchestrated by hepcidin. This hepatic peptide regulates iron homeostasis by occluding and/or degrading ferroportin, the sole known iron exporter on the surface of macrophages, duodenal enterocytes and other iron storage cells (Xiao, Alfaro-Magallanes, & Babitt, 2020).
Iron balance and iron supplementation for the female athlete: A practical approach
Published in European Journal of Sport Science, 2018
Charles R Pedlar, Carlo Brugnara, Georgie Bruinvels, Richard Burden
The regulation of iron absorption, storage and the regulation of erythropoiesis is under the control of iron protein regulators and hypoxia inducible factors respectively (Kuhn, 2015). Iron absorption is under the control of the peptide hormone hepcidin which was only relatively recently discovered (Nemeth et al., 2004). Briefly, hepcidin is secreted in the liver and increases in response to iron overload (Burden, Morton, Richards, Whyte, & Pedlar, 2015) or inflammation, shutting down iron absorption via ferroportin. Conversely, hepcidin decreases in anaemia, promoting iron absorption. Since exercise results in an inflammatory response, it can transiently increase hepcidin (Burden, Pollock, et al., 2015), potentially reducing the capacity to absorb iron. Therefore, heavy and frequent exercise training bouts may put the athlete at risk of iron deficiency although more studies are needed to understand the longitudinal effects of exercise upon hepcidin. Recent evidence suggests that during recovery from marathon training iron status improves (Pedlar et al., 2017), thus, rest may be an effective means of correcting iron deficiency although more studies are needed.
Hepcidin and interleukin-6 responses to endurance exercise over the menstrual cycle
Published in European Journal of Sport Science, 2022
Laura Barba-Moreno, Víctor M. Alfaro-Magallanes, Xanne A.K. Janse de Jonge, Angel E. Díaz, Rocío Cupeiro, Ana B. Peinado
Exercise is known to increase the cytokine Interleukin-6 (IL-6) (Pedersen, Steensberg, & Schjerling, 2001), which has been reported to be one of the main regulators of the iron regulatory hormone hepcidin (Nemeth et al., 2004). Hepcidin is a peptide hormone secreted by the liver, which regulates iron homeostasis by binding to ferroportin, inducing its internalization and degradation and modulating duodenal iron absorption and recycling in macrophages (Pedersen et al., 2001, Peeling et al., 2008, 2009a).