Tmprss6 Is a Genetic Modifier of the Hfe-Hemochromatosis Phenotype in Mice.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 625-625
Author(s):  
Karin E. Finberg ◽  
Rebecca Whittlesey ◽  
Mark D. Fleming ◽  
Nancy C. Andrews
Keyword(s):  
Iron Deficiency ◽  
Iron Content ◽  
Serum Iron ◽  
Iron Concentration ◽  
Transferrin Saturation ◽  
Heme Iron ◽  
Deficiency Anemia ◽  
Wild Type ◽  
Non Heme Iron ◽  
Serum Iron Concentration

Abstract Abstract 625 HFE-associated hereditary hemochromatosis is an autosomal recessive disorder characterized by inappropriately elevated absorption of dietary iron by the gastrointestinal mucosa, resulting in excessive storage of iron in multiple organs. A significant proportion of individuals who are homozygous for HFE mutations fail to develop clinical symptoms, suggesting that environmental and/or genetic factors may influence the penetrance of this disorder. In vitro and animal studies have revealed that HFE promotes the expression of hepcidin, a circulating hormone produced by the liver that acts to inhibit iron absorption by the duodenum. In contrast, TMPRSS6, a transmembrane serine protease produced by the liver, acts to inhibit hepcidin expression; both humans and mice harboring TMPRSS6 mutations display impaired intestinal iron absorption, resulting in a phenotype of iron-refractory iron deficiency anemia (IRIDA). Here we asked if heterozygous or homozygous loss of Tmprss6 function could modify the iron overload phenotype of Hfe null (Hfe-/-) mice, a mouse model of human HFE-hemochromatosis. To test this, we bred Hfe-/- mice to Tmprss6-/- mice; the latter harbor a targeted disruption of the Tmprss6 serine protease domain and exhibit an IRIDA phenotype. We generated Hfe-/-Tmprss6+/+, Hfe-/-Tmprss6+/-, and Hfe-/-Tmprss6-/- female mice (6-10 mice per genotype), in which parameters of systemic iron homeostasis were compared at eight weeks of age by Student's t test. Consistent with previous study of Hfe-/- mice, Hfe-/- mice harboring two wild type Tmprss6 alleles (Hfe-/-Tmprss6+/+ mice) showed serum iron concentration, transferrin saturation, and hepatic non-heme iron content that were significantly elevated compared to wild type mice of similar genetic background. Heterozygosity for Tmprss6 mutation, however, markedly reduced the severity of the hemochromatosis phenotype of Hfe-/- mice. Compared to Hfe-/- mice with two wild type Tmprss6 alleles, Hfe-/- mice that were heterozygous for Tmprss6 mutation (Hfe-/-Tmprss6+/- mice) showed significant reductions in serum iron concentration (p<0.01), transferrin saturation (p<0.005), and non-heme iron content of liver (p<10-4). Furthermore, homozygosity for Tmprss6 mutation completely ameliorated the iron overload phenotype of Hfe-/- mice and in fact led to systemic iron deficiency. Compared to both Hfe-/-Tmprss6+/+ and Hfe-/-Tmprss6+/- mice, Hfe-/-Tmprss6-/- mice showed markedly reduced serum iron concentration (p<10-7), transferrin saturation (p<10-10), and non-heme iron content of liver (p<10-4). Hfe-/-Tmprss6-/- mice also displayed iron deficiency anemia and appeared phenotypically similar to previously characterized Tmprss6-/- mice harboring two wild type copies of Hfe. In summary, these results demonstrate that Tmprss6 is a genetic modifier of the Hfe-hemochromatosis phenotype in mice. These findings suggest that natural genetic variation in the human ortholog TMPRSS6 might modify the clinical penetrance of HFE-hemochromatosis and raise the possibility that pharmacological inhibition of TMPRSS6 activity might prove an effective therapy in this disorder. Disclosures: No relevant conflicts of interest to declare.

Abdominal Chronic Expanding Hematoma Causing Iron-Deficiency Anemia in a Dog

2014 ◽  
Vol 50 (5) ◽  
pp. 350-355 ◽  
Author(s):  
Lionel Sebbag ◽  
Kenneth R. Harkin ◽  
Allison Habekost ◽  
Sanjeev Gumber ◽  
Tiffany Lee
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Serum Iron ◽  
Abdominal Cavity ◽  
Iron Concentration ◽  
Abdominal Distention ◽  
Deficiency Anemia ◽  
Surgical Removal ◽  
Chronic Expanding Hematoma ◽  
Serum Iron Concentration

A 2 yr old spayed female mixed-breed Irish wolfhound was referred for assessment of anemia and slowly progressing abdominal distention. At the time of admission, the dog had marked anemia and thrombocytosis, a decreased serum iron concentration, and a normal coagulation profile. An ultrasound examination showed a massive fluid-filled cavitated structure in the abdominal cavity. Paracentesis of that structure yielded a large amount of hemorrhagic fluid with an iron concentration &gt;24 times greater than the serum iron concentration, consistent with chronic sequestration of iron, leading to iron-deficiency anemia. Blood transfusions and incomplete surgical removal of the structure allowed short-term stabilization of the patient, but the dog was euthanized 17 days postsurgery for lethargy and continued abdominal distention. Histopathological evaluation of the structure was consistent with a chronic expanding hematoma. To the authors’ knowledge, this is the first reported case of intra-abdominal chronic expanding hematoma in a dog. It is also unique given its features of iron-deficiency anemia caused by internal blood loss.

Iron Deficiency Anemia Following Prenatal Nutrition Interventions

2007 ◽  
Vol 68 (4) ◽  
pp. 222-225
Author(s):  
Caroline P. Leblanc ◽  
France M. Rioux
Keyword(s):  
Iron Deficiency ◽  
Pregnant Women ◽  
Iron Deficiency Anemia ◽  
Low Income ◽  
Mean Corpuscular Volume ◽  
Serum Iron ◽  
Transferrin Saturation ◽  
Deficiency Anemia ◽  
Corpuscular Volume ◽  
Prevalence Of Anemia

Purpose: Iron deficiency anemia (IDA) during pregnancy and infancy is still common in developed countries, especially in low-income groups. We examined the prevalence of anemia and IDA in healthy low-income pregnant women participating in the Early Childhood Initiatives (ECI) program, and in their infants when they reached six months of age. Methods: Pregnant women were recruited by nutritionists. In mothers, hemoglobin (Hb), mean corpuscular volume, and serum ferritin (SF) were measured at 36 ± 2 weeks of gestation. In infants, Hb, mean corpuscular volume, SF, serum iron, total iron binding capacity (TIBC), and transferrin saturation (TS) were measured at six months of age. Thirty-one mother-infant pairs participated. Results: Among the 31 pregnant women participating in the ECI program, six (19.4%) were anemic (Hb <110 g/L) and five (16.1%) suffered from IDA (Hb <110 g/L and SF <10 µg/L). Among infants, seven of 23 (30.4%) were anemic (Hb <110 g/L) and five of 23 (21.7%) suffered from IDA (Hb <110 g/L plus two of the following: TIBC >60 µmol/L, SF <10 µg/L, serum iron <5.3 µmol/L, TS ≤15%). Conclusions: The prevalence of anemia in this group of lowincome pregnant women is comparable to that in privileged women. The prevalence of IDA in infants is comparable to that observed in other high-risk groups. Effective strategies are needed to prevent IDA in vulnerable groups.

RNAi-Mediated Inhibition of Tmprss6 Elevates Hamp1 Expression and Reduces Serum Iron Levels in Mice

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1045-1045 ◽  
Author(s):  
Ivanka Toudjarska ◽  
Zuhua Cai ◽  
Tim Racie ◽  
Stuart Milstein ◽  
Brian R Bettencourt ◽  
...  
Keyword(s):  
Iron Overload ◽  
Serum Iron ◽  
Iron Concentration ◽  
Transferrin Saturation ◽  
Elevated Serum ◽  
High Serum ◽  
Therapeutic Modality ◽  
Deficiency Anemia ◽  
Loss Of Function ◽  
Hepcidin Expression

Abstract Abstract 1045 The liver hormone Hepcidin (encoded by Hamp1) regulates serum iron levels by controlling the efflux of iron from intestinal enterocytes and macrophages. Maintaining sufficient iron levels to support erythropoiesis while preventing iron overload requires tight control of Hepcidin expression. Transcription of Hamp1 in hepatocytes is stimulated by high serum iron levels, via Transferrin Receptor signaling, as well as by activation of the BMP/SMAD pathway. The membrane serine protease Matriptase-2 (encoded by Tmprss6) inhibits BMP induced Hamp1 induction through the regulation of the BMP co-receptor, Hemojuvelin. In humans, loss of function mutations in TMPRSS6 lead to elevated Hepcidin levels resulting in iron-resistant iron-deficiency anemia (IRIDA). In diseases associated with iron overload, such as Thalassemia intermedia (TI) and Familial Hemochromatosis (FH), Hepcidin levels are low despite elevated serum iron concentrations. Studies in murine models of TI and FH have shown that elevating Hepcidin levels by genetic inactivation of Tmprss6 can prevent iron overload and correct aspects of the disease phenotype. Therefore, therapeutic strategies aimed at specifically inhibiting Tmprss6 expression could prove efficacious in these, and other, iron overloading diseases. Here we show that systemic administration of a potent lipid nanoparticle (LNP) formulated siRNA directed against Tmprss6 leads to durable inhibition of Tmprss6 mRNA in the mouse liver, with concomitant elevation of Hamp1 expression. This leads to significant decreases in serum iron concentration and Transferrin saturation, along with changes in hematologic parameters consistent with iron restriction. Further testing in mouse genetic models of TI and FH will support the rationale for developing LNP formulated Tmprss6 siRNA as a novel therapeutic modality. Disclosures: Toudjarska: Alnylam Pharmaceuticals, Inc.: Employment. Cai:Alnylam Pharmaceuticals, Inc.: Employment. Racie:Alnylam Pharmaceuticals, Inc.: Employment. Milstein:Alnylam Pharmaceuticals, Inc.: Employment. Bettencourt:Alnylam Pharmaceuticals, Inc.: Employment. Hettinger:Alnylam Pharmaceuticals, Inc.: Employment. Sah:Alnylam Pharmaceuticals, Inc.: Employment. Vaishnaw:Alnylam Pharmaceuticals, Inc.: Employment. Bumcrot:Alnylam Pharmaceuticals, Inc.: Employment.

scholarly journals Iron Deficiency Anemia Caused By Malabsorption from Proton Pump Inhibition

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 962-962
Author(s):  
Michael Boxer
Keyword(s):  
Iron Deficiency ◽  
Ferric Iron ◽  
Intravenous Iron ◽  
Heme Iron ◽  
Deficiency Anemia ◽  
Non Heme Iron ◽  
Clear Explanation ◽  
Iv Iron ◽  
Gastric Parietal Cells ◽  
Iron Replacement

Introduction: Iron deficiency anemia (IDA) not responding to oral iron replacement usually requires a hematologic evaluation. 48 patients taking a proton pump inhibitor (PPI) and not responding to oral iron replacement were found to have an elevated serum gastrin (SG). No patient had gastrointestinal bleeding, gastric resection, bariatric surgery, or menorrhagia. Other causes for iron malabsorption such as celiac disease or helicobacter infection were not present. 94 percent responded to intravenous iron (IV iron). Methods: All patients previously had undergone diagnostic gastrointestinal evaluations. Testing for celiac disease and helicobacter infection was negative. Gastric biopsies did not demonstrate atrophy. Most referrals were from gastroenterologists. Results: 94% responded to IV iron with a rise in their hemoglobin of &gt;/= 2 grams per cent. 83 percent (40/48) were women. Iron dextran (ID) at a fixed dose of 825 mgm was given to 85% of the patients. Twelve of these 41 patients were given a second infusion of ID as the first dose did not produce a satisfactory response. Ferric carboxymaltose and ferumoxytol were each given once at the fixed recommended dose, and second infusions was not necessary. Four patients received iron sucrose at a weight based dose, and a second series of infusions were not necessary. One patient responded to ferumoxytol after a suboptimal response to iron dextran. An elevated SG was defined as &gt;100 pg/mL. The average SG was 370.25 pg/mL (114 to 2101 pg/mL). Hemoglobin rose an average of 3.35 gram% (9.56 to 12.91 gm%). The change in hemoglobin was minus 0.4 to plus 7.0 gm% with a baseline hemoglobin ranging between 6.6 to 14.3 gm% and rising between 9.3 to 16.2 gram%. Ferritin rose an average of 14.8 to 158 ng/mL with baseline ferritin ranging between 3 to 73 ng/mL and rising between 22 to 659 ng/mL The average MCV rose from 75.89 to 84.93 fL with baseline MCV ranging between 61 to 93 fL rising between 69 to 96 fL The average iron saturation rose from 7.49 to 22.89% with baseline saturation ranging between 2 to 34% and rising between 10 to 39%. Discussion: Dietary iron consists of both heme and non heme iron. Heme iron is derived from the hemoglobin and myoglobin in animal food sources such as meat, seafood, and poultry. Heme iron is in the ferrous (II) oxidation state, is easily absorbable, and contributes 10% or somewhat more of total absorbed iron. Non heme iron is in the ferric (III) form and is derived from plants and iron fortified food. Normally 1-2 mgm of iron is absorbed daily. Heme iron is well absorbed after its release by pancreatic enzymes. Non heme iron is less well absorbed and requires acid secretion from gastric parietal cells for the denaturing of ingested proteins and subsequent proteolysis. PPI causes decreased hydrogen ion (H+) production by inhibiting the hydrogen/potassium pump within gastric parietal cells. The elevated SG derives from G cell hyperplasia as a response to the lowered H+ activity caused by PPI. The decreased H+ activity inhibits the release of ferric iron from non animal sources. Iron absorption occurs in the proximal duodenum through the action of a brush border ferrireductase such as duodenal cytochrome B which reduces ferric iron to ferrous iron. With less ferric iron available for reduction less ferrous iron is absorbed, and iron deficiency results. Intravenous iron fully corrected the IDA in 94% of treated patients. Two of the 3 non responders were obese and only received one infusion of ID. Perhaps a second infusion might have been beneficial. However no relation between weight, response, and ID dosing could be detected. Both patients had normal hemoglobins before the iron infusion but were very symptomatic from their iron deficiency. Both patients experienced a rise in their hemoglobin (1.9 gram% and 1.4 gm%). The third non responder actually had a fall in the hemoglobin from 10.5 to 10.1 gm%. No clear explanation was apparent. No clear explanation for the female predominance was apparent. Conclusion: In 2009 119 million prescriptions for PPI were written in the USA. The gastrointestinal literature suggests that anemia from PPI is uncommon. Very likely IDA due to IM from PPI is much more common than recognized and should be considered for any iron deficient patients without evidence for other causes for IDA. Intravenous iron is highly effective. Disclosures No relevant conflicts of interest to declare.

The Serine Protease Tmprss6 Regulates Hepcidin Expression, but Its Loss Does Not Cause Systemic Iron Deficiency In the Fetal and Neonatal Periods

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4258-4258
Author(s):  
Ramsey M. Wehbe ◽  
Rebecca L. Whittlesey ◽  
Nancy C. Andrews ◽  
Karin E. Finberg
Keyword(s):  
Iron Deficiency ◽  
Iron Homeostasis ◽  
Iron Concentration ◽  
Fold Increase ◽  
Heme Iron ◽  
Hepcidin Expression ◽  
Non Heme Iron ◽  
Iron Parameters ◽  
Maternal Iron ◽  
Hepcidin Mrna

Abstract Abstract 4258 Mutations in TMPRSS6 (matriptase-2), a transmembrane serine protease expressed by the liver, result in the clinical phenotype of iron refractory iron deficiency anemia (IRIDA). Additionally, common polymorphisms in TMPRSS6 have been associated with variation in laboratory parameters of iron homeostasis in healthy populations. TMPRSS6 increases iron absorption by reducing expression of the hepatic hormone, hepcidin, via down-regulation of a BMP/SMAD signaling cascade. Hepcidin promotes the internalization and degradation of the duodenal iron transporter, ferroportin, thereby inhibiting iron absorption. Previous studies have demonstrated that adult mice with Tmprss6 deficiency exhibit elevated hepatic hepcidin mRNA levels that are associated with decreased hepatic iron stores. In one study, genetic loss of Tmprss6 was shown to result in significant elevation of hepatic hepcidin expression in mice at birth; however, whether this hepcidin elevation was associated with abnormalities in iron homeostasis was not reported. We therefore asked if the elevated hepcidin levels present in newborn Tmprss6-/- pups correlate with abnormal parameters of iron homeostasis in the fetal or neonatal periods. To answer this question, we intercrossed Tmprss6+/− mice to generate Tmprss6+/+, Tmprss6+/−, and Tmprss6-/- progeny for phenotypic characterization at either gestational day 17.5 (E17.5) or postnatal day 0 (P0). Consistent with prior observations, Tmprss6-/- pups at P0 showed a 4.6-fold increase in hepatic hepcidin mRNA compared to Tmprss6+/+ littermates (p=.006). However, despite this elevation in hepcidin expression, Tmprss6-/- pups were not pale, and they showed no significant differences in body mass or hepatic non-heme iron concentration compared to Tmprss6+/+ and Tmprss6+/− littermates. At E17.5, Tmprss6-/- fetuses showed a 50-fold increase in hepatic hepcidin mRNA compared to Tmprss6+/+ littermates (p=.005). However, Tmprss6-/- fetuses also were not pale, and they showed no significant difference in body mass compared to Tmprss6+/+ and Tmprss6+/− littermates. Surprisingly, hepatic non-heme iron concentration at E17.5 was significantly higher in Tmprss6-/- fetuses than in Tmprss6+/+ fetuses (p=.003). To determine if the increased hepcidin expression of Tmprss6-/- fetuses might affect iron homeostasis in their pregnant mothers, we measured iron parameters in Tmprss6+/− females gestating E17.5 litters that were enriched for either Tmprss6+/+ or Tmprss6-/- fetuses. No significant effects of fetal genotype on maternal iron parameters were observed. In summary, our results demonstrate that Tmprss6 regulates hepcidin expression in the fetal and neonatal periods in mice. However, Tmprss6 deficiency does not appear to be associated with systemic iron deficiency at these stages of development, and fetal Tmprss6 expression does not have a significant effect on maternal iron homeostasis in late gestation. These results may have implications for understanding the maintenance of iron homeostasis in early development, and may provide insight into the evolution of IRIDA as well as other disorders of iron homeostasis. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Compound Heterozygous Hemochromatosis Genotype Predicts Increased Iron and Erythrocyte Indices in Women

2000 ◽  
Vol 46 (2) ◽  
pp. 162-166 ◽  
Author(s):  
Enrico Rossi ◽  
John K Olynyk ◽  
Digby J Cullen ◽  
George Papadopoulos ◽  
Max Bulsara ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Serum Iron ◽  
Transferrin Saturation ◽  
Hfe Gene ◽  
Compound Heterozygous ◽  
Age Group ◽  
Wild Type ◽  
C282y Mutation ◽  
Younger Age ◽  
Compound Heterozygotes

Abstract Background: Women who inherit heterozygosity for the C282Y mutation of the HFE gene may have increased serum iron indices and hemoglobin and are less likely to develop iron deficiency compared with women with the wild-type genotype. Methods: We performed a cross-sectional analysis of 497 women 20–44 years of age and 830 women &gt;51 years of age drawn from the Busselton (Australia) population study to assess the effects of the HFE genotype on serum iron and hematology indices. Results: Heterozygosity for the C282Y mutation occurred in 13.8% of the study population, comprising 11.8% C282Y wild-type heterozygotes and 2.0% C282Y/H63D compound heterozygotes. In the younger age group, C282Y wild-type women did not have significantly increased serum iron, transferrin saturation, or hemoglobin values, and were not protected from developing iron deficiency, compared with women of the same age with the wild-type genotype. Young compound heterozygous women had higher means for serum iron (25.0 vs 16.9 μmol/L; P &lt;0.001), transferrin saturation (42.0% vs 25.6%; P &lt;0.05), hemoglobin (139.4 vs 132.3 g/L; P &lt;0.05), and corpuscular volume (91.1 vs 87.7 fL; P &lt;0.05), and a higher median ferritin (53 vs 44 μg/L; P &lt;0.05) compared with the wild-type genotype. Similar results were observed for compound heterozygotes in the &gt;51 years age group. Conclusions: Women with the compound heterozygous HFE genotype C282Y/H63D, but not the C282Y wild-type genotype, had increased values for serum iron and transferrin saturation, and the younger age group also had increased hemoglobin values. We conclude that the compound heterozygous genotype may have a beneficial effect in protecting women from iron deficiency.

scholarly journals FORTIFIKASI GUAVA (Psidium guajava L.) JELLY DRINK DENGAN ZAT BESI ORGANIK DARI KEDELAI (Glycine max L.) DAN KACANG HIJAU (Vigna radiate L.)

2017 ◽  
Vol 11 (1) ◽  
pp. 10
Author(s):  
Christina Hanny Setyaningrum ◽  
Ivone Elizabeth Fernandez ◽  
Robertus Probo Yulianto Nugrahedi
Keyword(s):  
Ascorbic Acid ◽  
Iron Content ◽  
Extraction Process ◽  
Psidium Guajava ◽  
Heme Iron ◽  
The Body ◽  
Deficiency Anemia ◽  
Non Heme Iron ◽  
Glycine Max L ◽  
Nutrition Value

Anemia is a condition of haemoglobin level that is below normal. One of the major causes is lacking of iron consumption, which is important in haemoposis process. Compared to men, women have less total iron in the body, and it raises the risk of anemia. The main purpose of this research was the fortification of iron in beverage. This research used soybean and mungbean as source of iron, which known as non-heme iron. To improve the absorption, ascorbic acid was needed as an enhancer, using guava and was produced into guava jelly drink. Method for extraction process is by maseration with 30% etanol as solution. The value of iron extract assessed by AAS at 248,3 nm. The formula of fortification was 20% of RDA of iron for woman, which was 18 mg per day. Chosen product was evaluated by sensory test. The nutrition value of product assessed including iron content, ascorbic acid, and proximate composition. The iron content of soybean was 113,86 ppm and 58,76 for mungbean. The nutrition of guava jelly drink with addition of fortificant were 87,47% water, 0,35% ash, 0,2% fat, 0,31% protein, 11,67% carbohydrate, 130,48 ppm iron, and 90,79 mg ascorbic acid. Keywords: iron deficiency anemia, soy bean, mungbean, jelly drink, and guava

scholarly journals Systems genetic analysis of multivariate response to iron deficiency in mice

2012 ◽  
Vol 302 (11) ◽  
pp. R1282-R1296 ◽  
Author(s):  
Lina Yin ◽  
Erica L. Unger ◽  
Leslie C. Jellen ◽  
Christopher J. Earley ◽  
Richard P. Allen ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Principal Components ◽  
Qtl Analysis ◽  
Iron Homeostasis ◽  
Iron Concentration ◽  
Transferrin Saturation ◽  
Iron Regulation ◽  
Deficiency Anemia ◽  
Dietary Iron ◽  
Multiple Genes

The aim of this study was to identify genes that influence iron regulation under varying dietary iron availability. Male and female mice from 20+ BXD recombinant inbred strains were fed iron-poor or iron-adequate diets from weaning until 4 mo of age. At death, the spleen, liver, and blood were harvested for the measurement of hemoglobin, hematocrit, total iron binding capacity, transferrin saturation, and liver, spleen and plasma iron concentration. For each measure and diet, we found large, strain-related variability. A principal-components analysis (PCA) was performed on the strain means for the seven parameters under each dietary condition for each sex, followed by quantitative trait loci (QTL) analysis on the factors. Compared with the iron-adequate diet, iron deficiency altered the factor structure of the principal components. QTL analysis, combined with PosMed (a candidate gene searching system) published gene expression data and literature citations, identified seven candidate genes, Ptprd, Mdm1, Picalm, lip1, Tcerg1, Skp2, and Frzb based on PCA factor, diet, and sex. Expression of each of these is cis-regulated, significantly correlated with the corresponding PCA factor, and previously reported to regulate iron, directly or indirectly. We propose that polymorphisms in multiple genes underlie individual differences in iron regulation, especially in response to dietary iron challenge. This research shows that iron management is a highly complex trait, influenced by multiple genes. Systems genetics analysis of iron homeostasis holds promise for developing new methods for prevention and treatment of iron deficiency anemia and related diseases.

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