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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].
Nanoencapsulation of Iron for Nutraceuticals
Published in Bhupinder Singh, Minna Hakkarainen, Kamalinder K. Singh, NanoNutraceuticals, 2019
Naveen Shivanna, Hemanth Kumar Kandikattu, Rakesh Kumar Sharma, Teenu Sharma, Farhath Khanum
Hepcidin is important for control of iron absorption and metabolism. Its expression is controlled by the HAMP gene and is one of the small peptides with several isoforms. It is known to be predominantly expressed in the liver. As stated earlier, it is involved in maintaining iron homeostasis. It binds to cell surface ferroportin, resulting in phosphorylation of tyrosine residue further internalization, ubiquitination, and degradation. All these processes occur in lysosomes. Hepcidin has a significant role in inhibition of iron absorption, release of iron from macrophages, and is transported across the placenta. It is found as bound to a protein, α-2–macroglobulin in plasma, with its route of clearance through the kidney. Quantification of Hepcidin in serum and urine is carried out by ELISA or mass spectrophotometer techniques. Its concentrations become low and sometimes undetectable in conditions such as haemochromatosis and anemia, and become high in some cases such as inflammation.
Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
Hepcidin is a newly discovered short peptide found to possess antimicrobial and iron-regulatory functions. It can bind to M1P1 to regulate iron levels, and inflammation and elevated iron levels can induce hepcidin expression.167 They have shown that hepcidin is also expressed throughout the CNS and its expression increases with age. The widespread distribution of hepcidin in the brain and its presence in the peripheral organs implies that the peptide may also play a central role in brain iron homeostasis. They have also demonstrated that hepcidin may have unique functions in the brain, not only inhibiting iron release but also reducing uptake by downregulating DMT1 and TIR1 expression.168,169 Their data also suggest reduced net iron uptake in response to hepcidin treatment, which may help relieve iron overloading.168 It is not clear if hepcidin levels are altered in neurodegeneration characterized by brain iron accumulation. Further investigation is needed to assess the potential role of hepcidin in modifying iron-induced pathology.
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).
Military nutrition research: Contemporary issues, state of the science and future directions
Published in European Journal of Sport Science, 2022
J. Philip Karl, Lee M. Margolis, Joanne L. Fallowfield, Robert B. Child, Nicola M. Martin, James P. McClung
Suboptimal diet, poor health and the physical demands of military training and operations can result in an inflammatory response that effects nutrient absorption and homeostasis. Both excess body fat and physical activity stimulate the synthesis and circulation of inflammatory cytokines, such as interleukin-6 (IL-6), which in turn stimulates the expression of hepcidin by the liver. Hepcidin, a regulator of iron homeostasis, affects iron absorption at the gut, and basolateral iron export from both the enterocyte and macrophage through the degradation of the cellular iron exporter, ferroportin (Ganz & Nemeth, 2012). Diminished iron absorption and the sequestering of iron in cells due to inflammation results in functional deficits as iron becomes unavailable for incorporation into proteins and enzymes necessary to support physical function (e.g. haemoglobin and myoglobin for the transport and storage of oxygen). Poor iron status is a significant concern for military personnel as nearly 15% of female recruits experience poor iron status at accession to military service (McClung et al., 2006), iron status declines during military training and operations (McClung et al., 2009), and that decline is associated with reduced physical performance (McClung et al., 2009). Moreover, one recent applied study in military personnel demonstrated increased IL-6 and hepcidin following a short (4-day) training operation (Pasiakos et al., 2016). Interestingly, hepcidin concentrations were associated with energy deficit, suggesting that underfeeding may potentiate the inflammatory response to physically demanding training. That hypothesis is consistent with findings of a recent study wherein a 45% energy deficit potentiated increases in hepcidin, decreases in iron absorption (∼45% reduction), and increases in some, but not all, markers of inflammation during a 3-d simulated military training (Hennigar et al., 2021).