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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The important function of iron as a necessary nutrition element in mammals is more and more recognized by people. The normal physiological level of iron is ensured by the rigid regulation mechanism of iron metabolism in animals. Various clinical diseases are induced by iron disorder, like iron deficiency and iron overloading in the body. The current study showed that Hepcidin may be a key factor to control intestinal iron absorbing and regulates iron homeostasis, and may be an important regulating hormone of iron metabolism. It was summarized in this paper that the physiological functions, iron deficiency diseases, for instance iron deficiency anemia and neural diseases of children, and iron overload diseases, such as liver damage, cardiovascular diseases, Parkinson's disease, and cancers etc. And it was expected how to develop the therapy of iron disorder diseases in gene level use modern techniques.
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PMID:[Progress of the study on iron disorder diseases]. 1823 99

Meeting the iron requirements of infants and children is difficult, and supplementation or fortification of food with iron is often recommended. Although iron supplementation of infants and children with iron deficiency and iron-deficiency anemia may be beneficial, recent studies suggest that this may not be the case for those with adequate iron status, and adverse effects have been noted. The recent discoveries of proteins and peptides regulating iron absorption have enhanced our knowledge of iron metabolism in infants and children. Iron is taken up in the small intestine by divalent metal transporter-1 and is either stored by ferritin inside the mucosal cell or transported to the systemic circulation by ferroportin, while being oxidized by hephaestin to be incorporated into transferrin. Hepcidin, a small peptide synthesized by the liver, can sense iron stores and regulates iron transport by inhibition of ferroportin. However, regulation of iron transporters is immature in infants, possibly explaining the adverse effects of iron supplementation. Interactions among iron, vitamin A, zinc, and copper need to be considered when evaluating the effects of iron supplementation on infants and children.
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PMID:Iron metabolism in infants and children. 1829 87

Recently discovered peptide hormone hepcidin is the key regulator of systemic iron homeostasis. Iron metabolism is regulated in response to variations in hepcidin plasma levels. Hepcidin levels that are inappropriately low or high result in iron overload or iron deficiency, respectively. The early studies showed that hypoxia, iron concentration, and inflammation influence hepcidin levels, but the exact mechanism remained elusive. Very recently, different research groups discovered that IL-6, through the Jak/STAT-3 signaling pathway, is involved in regulation of hepcidin levels in response to inflammatory stimuli. In this review we present a general view of hepcidin biology, with emphasis on regulation in inflammatory conditions.
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PMID:IL-6 - STAT-3 - hepcidin: linking inflammation to the iron metabolism. 1833 66

Iron is utilised by the body for oxygen transport and energy production, and is therefore essential to athletic performance. Commonly, athletes are diagnosed as iron deficient, however, contrasting evidence exists as to the severity of deficiency and the effect on performance. Iron losses can result from a host of mechanisms during exercise such as hemolysis, hematuria, sweating and gastrointestinal bleeding. Additionally, recent research investigating the anemia of inflammation during states of chronic disease has allowed us to draw some comparisons between unhealthy populations and athletes. The acute-phase response is a well-recognised reaction to both exercise and disease. Elevated cytokine levels from such a response have been shown to increase the liver production of the hormone Hepcidin. Hepcidin up-regulation has a negative impact on the iron transport and absorption channels within the body, and may explain a potential new mechanism behind iron deficiency in athletes. This review will attempt to explore the current literature that exits in this new area of iron metabolism and exercise.
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PMID:Athletic induced iron deficiency: new insights into the role of inflammation, cytokines and hormones. 1836 40

Hepcidin, a liver-derived protein that restricts enteric iron absorption, is the key regulator of body iron content. Several proteins induce expression of the hepcidin-encoding gene Hamp in response to infection or high levels of iron. However, mechanism(s) of Hamp suppression during iron depletion are poorly understood. We describe mask: a recessive, chemically induced mutant mouse phenotype, characterized by progressive loss of body (but not facial) hair and microcytic anemia. The mask phenotype results from reduced absorption of dietary iron caused by high levels of hepcidin and is due to a splicing defect in the transmembrane serine protease 6 gene Tmprss6. Overexpression of normal TMPRSS6 protein suppresses activation of the Hamp promoter, and the TMPRSS6 cytoplasmic domain mediates Hamp suppression via proximal promoter element(s). TMPRSS6 is an essential component of a pathway that detects iron deficiency and blocks Hamp transcription, permitting enhanced dietary iron absorption.
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PMID:The serine protease TMPRSS6 is required to sense iron deficiency. 1845 Dec 67

Hepcidin is a small protein comprised of 25 amino acids, synthesized in the liver. It was first described in 2001 as a component of the innate immunity due to its antimicrobial activity. Soon after, hepcidin was recognized as a key component in iron homeostasis, involved in maladies of iron overload or iron deficiency. Hepcidin acts by binding to the transmembrane protein ferroportin, in charge of exporting iron from cells. Upon binding to ferroportin, the latter is internalized into cytoplasmic lysosomes and is hydrolyzed, thus iron is accumulating in cells, and hypoferremia ensues. In hereditary and juvenile types of hemochromatosis, iron overload could be partially due to the down-regulation of hepcidin by the mutated genes HFE and HJV. In ferroportin disease, hepcidin synthesis is not inhibited, yet cells are still overloaded with iron due to mutations in ferroportin, preventing the binding of hepcidin and iron export from cell to the blood. Hepcidin has also been implicated in the scenario related to as "anemia of inflammation". In this condition significant hypoferremia develops as a result of acute sepsis, but also in wake of infections, chronic inflammation, rheumatic diseases and in certain malignancies. Such scarcity of iron leads to anemia that may not be corrected by erythropoietin treatment, and hepcidin synthesis in such anemic state is dramatically elevated. Future therapeutic approach may attempt administering synthetic hepcidin, or its antagonists, to correct states of iron overload or scarcity.
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PMID:[Hepcidin--the discovery of a small protein with a pivotal role in iron homeostasis]. 1848 71

Hepcidin has recently been recognized as a hormone essential to the negative regulation of iron. Synthesis of hepcidin is increased by iron overload or inflammation, and decreased by iron deficiency, anemia and erythropoietin. Dialysis patients frequently suffer the effects of both hepcidin increasing and decreasing factors. In this study, we investigated, for the first time, pro-hepcidin in dialysis patients while minimizing or manipulating these factors. We measured the serum pro-hepcidin in 23 hemodialysis patients without inflammation (the HD group) and 10 age-matched healthy volunteers. Those patients in the HD group were assigned to an iron-deficiency group (the ID group) or a non-iron deficiency subgroup (non-ID group). The HD group was followed up for two months. Iron therapy was performed in the ID group during the follow-up period. At the end of this time we evaluated the influence of iron therapy. Pro-hepcidin was similar in the HD groups and the healthy controls (295.1 [241.9, 413.7] vs. 301.7 [280.5, 383.5] ng/mL; not significant) despite the presence of hepcidin-decreasing factors. Pro-hepcidin in the ID group was significantly lower than in the non-ID group (262.6 [233.1, 295.1] vs. 359.2 [282.3, 446.5] ng/mL; P < 0.05). In patients newly acquiring ID during follow-up without iron supplementation, pro-hepcidin fell significantly (from 444.7 [389.4, 470.1] to 299.8 [233.4, 330.4] ng/mL; P < 0.05). Pro-hepcidin also showed an increase after ID was treated with iron administration (from 246.9 [205.5, 329.1] to 344.6 [290.1, 377.9] ng/mL; not significant). Pro-hepcidin could serve as a marker for functional iron deficiency and disordered iron utilization in HD. Underlying mechanisms and improvements in measurement techniques will require additional investigation.
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PMID:Serum pro-hepcidin as an indicator of iron status in dialysis patients. 1893 30

Hepcidin, the systemic regulator of iron homeostasis is activated by proteins responsible for hereditary hemochromatosis, bone morphogenetic proteins (BMPs), and inflammatory cytokines. Three recent publications now identify a novel hepcidin suppressor, the transmembrane serine protease TMPRSS6 (also known as matriptase-2), which is required to sense iron deficiency.
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PMID:Fine tuning of hepcidin expression by positive and negative regulators. 1859 Jun 84

Iron is an element which is essential to life but also potentially toxic. Therefore, clever mechanisms exist in the human body for uptake, transport and storage of iron. Hepcidin, which seems to be the master protein for regulation of intestinal iron absorption, is known for a short time. The expression of hepcidin is not only influenced by iron levels but also by mediators of inflammation and growth factors of erythropoiesis. Hence hepcidin plays also a crucial role in the development of anemia of chronic disease and iron overload due to ineffective erythropoiesis. Serum ferritin is a reliable parameter to estimate the storage iron. It is an acute phase protein which is elevated during infections and inflammations, though. In these situations, measurement of soluble transferrin receptors is a useful tool to differentiate between iron deficiency and anemia of chronic disease. Newer parameters as erythrocyte zink protoporphyrin or percentage of hypochromic erythrocytes (%HYPO) are suited to detect a functional iron deficiency. Early diagnosis of iron overload is essential to prevent organ damage. Serum ferritin and transferrin are useful parameters to screen for iron overload. If no clear reason for a secondary iron overload can be found, the search for a hereditary haemochromatosis is recommended. Most of these hereditary haemochromatoses are a result of mutations in the HFE gene (homozygous state for Cys282Tyr or compound heterozygosity for Cys282Tyr/ His63Asp) which can be detected by PCR technique. Liver biopsy is still the gold standard for quantification of storage iron. However, a method of increasing importance for quantification of iron overload is magnetic resonance imaging with new approaches as for example T2*.
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PMID:[Old and new iron parameters in iron metabolism and diagnostics]. 1879 66

Iron deficiency relatively observed in pregnant women is assumed to be enhanced by cigarette smoking. Hepcidin, a peptide hormone produced by the liver as pro-hepcidin, has recently emerged as a central mediator of iron metabolism. Hepcidin regulates intestinal iron absorption, macrophage iron release, and the placental passage of iron. Maternal smoking is associated with increased fetal iron requirements and stimulates fetal erythropoiesis. This is probably through a hypoxic effect on the fetus, and is dose related to the maternal smoking level. It is known that anemia and hypoxia suppress hepcidine mRNA expression. Therefore the aim of the study was to estimate the effect of tobacco smoking on serum pro-hepcidin levels and some iron parameters in pregnant women and umbilical cord blood. We also studied correlation between pro-hepcidin and others iron markers in mothers and their newborns. Healthy, pregnant women (n = 50), patients of Clinical Department of Obstetrics and Gynecology, Institute of Mother and Child were divided into groups nonsmoking and smoking according to questionnaire declaration. Serum concentrations of pro-hepcidin were determined by immunoenzymathic method using a commercial pro-hepcidin assay (DRG, Germany). Levels of ferritin and transferrin were measured by immunoturbidimetric method and iron by photometric test with ferrozine using HORIBA ABX kits (France) and Cobas Mira analyser (Roche, Switzerland). Levels of hemoglobin and hematocrite were determined using commercially available kits on Pentra 60 analyser (ABX, France). We observed that the mean concentration of pro-hepcidin in serum of smoking pregnant women was statistically lower than in tobacco abstinent (101.9 +/- 28.6 ng/ml vs 88.3 +/- 18.2 ng/ml; p < 0.01). Levels of others studied iron markers were similar in both group except total iron concentration, which was 20% lower in smoking mothers than in nonsmoking ones. In umbilical cord blood of infants born to smoking women level of pro-hepcidin was significantly lower than in tobacco abstinent (54.2 +/- 14.0 ng/ml vs 76.8 +/- 21.4 ng/ml, p < 0.0001). We observed positive correlation between concentrations of that prohormone in serum of mothers and cord blood of their newborns in nonsmoking group (r = 0.54; p < 0.02) as well as in smoking ones (r = 0.68; p < 0.05). In addition, concentrations of ferritin, transferin and total iron were lower by 30%, 13% and 20% respectively in cord blood of smoking than nonsmoking group. The differences were statistically significant (p < 0.05). Our analysis revealed no correlation between serum pro-hepcidin levels and other studied parameters of iron status both in the mothers and children groups. Our results indicate that tobacco smoking during pregnancy affected pro-hepcidine levels in serum of mothers and their newborns. Low concentrations of some iron markers in umbilical cord blood suggest that mother's smoking could lead to subclinical iron deficiency in fetus. No anemia were observed in both studied groups of mothers that could explain no relationships between pro-hepcidin and others parameters of iron status.
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PMID:[The effect of tobacco smoking during pregnancy on concentration of pro-hepcidin and some parameters of iron metabolism in matched-maternal cord pairs]. 1918 26


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