However, induction of more severe iron deficiency in human trophoblast in vitro resulted in the regulation of both TFR1 and FPN, similar to what was observed in the mouse model.
Our data demonstrate that elevated DNA methylation of the Hamp promoter region suppresses its expression, this epigenetic modification likely occurs in reaction to iron deficiency after bariatric surgery, helping to maintain system iron homeostasis.
In children with anaemia, rates of iron deficiency (low ferritin based on inflammation status, and/or high soluble transferrin receptor, ≥1.97 mg/L) and zinc deficiency (serum zinc <65 μg/dl) were 81.1% and 53.7%, respectively.
The discovery of hepcidin and its role in iron homeostasis has revolutionized our understanding of the pathogenesis of iron deficiency and iron overload states.
A proposed new mechanism of exercise-induced iron deficiency in athletes involves the iron-regulatory hormone hepcidin, however, there is limited information on this amongst elite athletes.
Iron deficiency increases FGF23 mRNA expression and recent evidence suggests that the recurrent, late-onset, or waxing-waning hypophosphatemic phenotype may be linked to synchronous variations in iron status.
Expression of hepcidin, the hormone regulating iron homeostasis, is increased by iron overload and decreased by accelerated erythropoiesis or iron deficiency.
High-dose erythropoietin (EPO) administration to hemodialysis (HD) patients with EPO hyporesponsiveness, due to iron deficiency, hyperparathyroidism, malnutrition, inflammation, and inadequate HD, results in increased risk of mortality and cardiovascular events.
Therefore, we aimed to determine the associations between iron deficiency and higher EPO levels with mortality, and the potential mediating role of FGF23, in a cohort of community-dwelling subjects.
Infants of mothers with the lowest levels of circulating hepcidin during gestation, likely a marker for iron deficiency, had higher sTfR:SF levels and lower hemoglobin levels, particularly at 12 months of age.
The purpose of this manuscript is to summarize current standard tools for identifying iron deficiency in anemic patients; explore the tools and context for evaluating novel markers, such as hepcidin, erythroferrone, and markers of the iron restriction response; and assess available evidence for how their use could increase our understanding of health outcomes in clinically challenging cases.
Under physiologic conditions, hepcidin production is reduced by iron deficiency and erythropoietic drive to increase the iron supply when needed to support red blood cell production and other essential functions.
The results showed that split iron supplementation efficiently improved hematological status of piglets and attenuated the induction of hepcidin expression, which resulted in the recovery of piglets from iron deficiency and the increase of iron utilization.
Earlier studies adjusted for CKD-mineral bone disease (CKD-MBD) regulators of FGF23 rather than for recently discovered non-CKD-MBD regulators, among which iron deficiency and heart failure are of particular importance.
Tmprss6-/- mice showed frank iron deficiency and reduced iron levels in most tissues, consistent with FPN playing an important role in the distribution of this metal, but manganese levels were largely unaffected.
Serum hepcidin levels and CHr were assessed in 65 early phase CHC patients (20 nonanemic, 23 anemic nonbleeders, and 22 anemic bleeders), and 20 healthy controls; and were compared with the conventional indices of iron deficiency including mean corpuscular volume, mean corpuscular hemoglobin, red cell distribution width, serum iron, total iron binding capacity, transferrin saturation and ferritin.
Therefore, we aimed to determine the associations between iron deficiency and higher EPO levels with mortality, and the potential mediating role of FGF23, in a cohort of community-dwelling subjects.
This study is aimed at investigating ID with conventional (ferritin, transferrin saturation [TSAT]) and new biomarkers (soluble transferrin receptor [sTfR], sTfR/log ferritin, reticulocyte hemoglobin content [CHr], hepcidin-25) in patients sub-grouped by the presence or absence of H. pylori infection.
The study found a significant correlation between serum hepcidin and iron deficiency-related parameters with adjustment for study groups (<i>p</i><.01).
Erythro-myeloid progenitors expressed less transferrin-receptor on the cell surface and had less labile iron compared to primitive erythroid progenitors, which could reduce their capacity to compete for scarce iron and survive iron deficiency.