Dietary and Physiological Factors That Affect the Absorption and Bioavailability of Iron

2005 ◽  
Vol 75 (6) ◽  
pp. 375-384 ◽  
Author(s):  
Janet R. Hunt

Iron deficiency, a global health problem, impairs reproductive performance, cognitive development, and work capacity. One proposed strategy to address this problem is the improvement of dietary iron bioavailability. Knowledge of the molecular mechanisms of iron absorption is growing rapidly, with identification of mucosal iron transport and regulatory proteins. Both body iron status and dietary characteristics substantially influence iron absorption, with minimal interaction between these two factors. Iron availability can be regarded mainly as a characteristic of the diet, but comparisons between human studies of iron availability for absorption require normalization for the iron status of the subjects. The dietary characteristics that enhance or inhibit iron absorption from foods have been sensitively and quantitatively determined in human studies employing iron isotopes. People with low iron status can substantially increase their iron absorption from diets with moderate to high availability. But while iron supplementation and fortification trials can effectively increase blood indices of iron status, improvements in dietary availability alone have had minimal influence on such indices within several weeks or months. Plentiful, varied diets are the ultimate resolution to iron deficiency. Without these, more modest food-based approaches to human iron deficiency likely will need to be augmented by dietary iron fortification.

Author(s):  
Satya Prasad Dixit ◽  
Logesh Rajan ◽  
Dhanabal Palaniswamy ◽  
Suresh Kumar Mohankumar

: Iron is one of the essential elements required for human health, as it plays a vital role in a number of metabolic, growth and developmental processes, including erythropoiesis, DNA synthesis, electron transport and others. Iron deficiency is a concern in both developing and developed (industrialized) countries, and in particular young women are highly vulnerable. This review investigates dietary and genetic determinants of iron metabolism in the human body and a possible solution to combat the iron deficiency by exploring via various targets. Hence, this review mainly focuses on the assessment of dietary and genetic factors affecting the iron bioavailability and homeostasis and collates the available information from 2000 to till date from Pubmed. The dietary factors including ascorbic acid an important factor in animal protein foods (meat, fish and poultry) enhance iron absorption whereas the phytic acid, soy protein, calcium and polyphenols have been reported to inhibit iron absorption. However, the effects of these dietary factors on iron absorption do not necessarily translate into an association with iron status and iron stores (serum ferritin concentration). Moreover, the genetic factors influence the absorption of iron involving HFE, TFR2, FPN1 and HAMP in humans. Further research is needed to determine optimal dietary recommendations for both the prevention and treatment of iron deficiency.


2019 ◽  
Vol 41 (1) ◽  
pp. 121-130 ◽  
Author(s):  
Susan Fairweather-Tait ◽  
Cornelia Speich ◽  
Comlan Evariste S. Mitchikpè ◽  
Jack R. Dainty

Background: Reference intakes for iron are derived from physiological requirements, with an assumed value for dietary iron absorption. A new approach to estimate iron bioavailability, calculated from iron intake, status, and requirements was used to set European dietary reference values, but the values obtained cannot be used for low- and middle-income countries where diets are very different. Objective: We aimed to test the feasibility of using the model developed from United Kingdom and Irish data to derive a value for dietary iron bioavailability in an African country, using data collected from women of child-bearing age in Benin. We also compared the effect of using estimates of iron losses made in the 1960s with more recent data for whole body iron losses. Methods: Dietary iron intake and serum ferritin (SF), together with physiological requirements of iron, were entered into the predictive model to estimate percentage iron absorption from the diet at different levels of iron status. Results: The results obtained from the 2 different methods for calculating physiological iron requirements were similar, except at low SF concentrations. At a SF value of 30 µg/L predicted iron absorption from the African maize-based diet was 6%, compared with 18% from a Western diet, and it remained low until the SF fell below 25 µg/L. Conclusions: We used the model to estimate percentage dietary iron absorption in 30 Beninese women. The predicted values agreed with results from earlier single meal isotope studies; therefore, we conclude that the model has potential for estimating dietary iron bioavailability in men and nonpregnant women consuming different diets in other countries.


2004 ◽  
Vol 23 (3) ◽  
pp. 279-283
Author(s):  
Bisera Atanasova ◽  
Robert Simpson ◽  
Andy Li ◽  
Kamen Tzatchev ◽  
Timothy Peters

Iron is a vital element for almost all living organisms. In mammals iron is taken by the intestinal epithelium, primarily in the duodenum. The initial step of absorption involves the reduction of ferric to ferrous iron both in gastric lumen and at the brush-border apical membrane. Reductase activity is increased by factors physiologically stimulating iron absorption, such as iron deficiency and chronic hypoxia. Ascorbic acid (Vitamin C) has long been known to enhance absorption of dietary iron in humans as shown by several nutritional/dietetic studies. This effect has been ascribed to lumenal reduction and solubilization of iron. Recent molecular cloning of the mammalian duodenal brush-border reductase activity has provided evidence that ascorbate may play an intracellular role in determining iron absorption rates. Previously, ascorbate concentrations have been determined in duodenum, but only in normal subjects and there is no evidence on how duodenal ascorbate alters in relation to intestinal iron absorption. The aim of this study is to examine mucosal and plasma levels of ascorbate and dehydroascorbate in normal subjects and patients with iron deficiency that is known to be a stimulator for iron absorption. Duodenal biopsies were homogenized in 5% metaphosphoric acid using single burst homogeniser. Tissue and plasma ascorbate levels were assayed by ferrozine spectrophotometric method. Blood was taken from each subject to assess the iron status. The analyses of human samples revealed increased duodenal (p <0.001, n = 20) and plasma (p <0.001, n = 6) ascorbate levels in patients with iron deficiency. These findings support an important intracellular role of ascorbic acid in human dietary iron absorption.


2017 ◽  
Vol 71 (Suppl. 3) ◽  
pp. 40-48 ◽  
Author(s):  
Andrew M. Prentice

The fact that humans must balance their need for iron against its potential for causing harm has been known for several centuries, but the molecular mechanisms by which we achieve this feat have only been revealed in the last 2 decades. Chief amongst these is the discovery of the master-regulatory liver-derived hormone hepcidin. By switching off ferroportin in enterocytes and macrophages, hepcidin exerts fine control over both iron absorption and its distribution among tissues. Hepcidin expression is downregulated by low iron status and active erythropoiesis and upregulated by iron overload and infection and/or inflammation. The latter mechanism explains the etiology of the anemia of chronic infection. Pharmaceutical companies are actively developing hepcidin agonists and antagonists to combat iron overload and anemia, respectively. In a global health context the discovery of hepcidin shines a new light on the world's most prevalent micronutrient problem; iron deficiency and its consequent anemia. It is now apparent that humans are not poorly designed to absorb dietary iron, but rather are exerting a tonic downregulation of iron absorption to protect themselves against infection. These new insights suggest that interventions to reduce infections and inflammation will be at least as effective as dietary interventions and that the latter will not succeed without the former.


2018 ◽  
Vol 108 (6) ◽  
pp. 1324-1333 ◽  
Author(s):  
Diego Moretti ◽  
Samuel Mettler ◽  
Christophe Zeder ◽  
Carsten Lundby ◽  
Anneke Geurts-Moetspot ◽  
...  

ABSTRACT Background Iron status is a determinant of physical performance, but training may induce both low-grade inflammation and erythropoiesis, exerting opposing influences on hepcidin and iron metabolism. To our knowledge, the combined effects on iron absorption and utilization during training have not been examined directly in humans. Objective We hypothesized that 3 wk of exercise training in recreational male runners would decrease oral iron bioavailability by increasing inflammation and hepcidin concentrations. Design In a prospective intervention, nonanemic, iron-sufficient men (n = 10) completed a 34-d study consisting of a 16-d control phase and a 22-d exercise-training phase of 8 km running every second day. We measured oral iron absorption and erythroid iron utilization using oral 57Fe and intravenous 58Fe tracers administered before and during training. We measured hemoglobin mass (mHb) and total red blood cell volume (RCV) by carbon monoxide rebreathing. Iron status, interleukin-6 (IL-6), plasma hepcidin (PHep), erythropoietin (EPO), and erythroferrone were measured before, during, and after training. Results Exercise training induced inflammation, as indicated by an increased mean ± SD IL-6 (0.87 ± 1.1 to 5.17 ± 2.2 pg/mL; P < 0.01), while also enhancing erythropoiesis, as indicated by an increase in mean EPO (0.66 ± 0.42 to 2.06 ± 1.6 IU/L), mHb (10.5 ± 1.6 to 10.8 ± 1.8 g/kg body weight), and mean RCV (30.7 ± 4.3 to 32.7 ± 4.6 mL/kg) (all P < 0.05). Training tended to increase geometric mean iron absorption by 24% (P = 0.083), consistent with a decreased mean ± SD PHep (7.25 ± 2.14 to 5.17 ± 2.24 nM; P < 0.05). The increase in mHb and erythroid iron utilization were associated with the decrease in PHep (P < 0.05). Compartmental modeling indicated that iron for the increase in mHb was obtained predominantly (>80%) from stores mobilization rather than from increased dietary absorption. Conclusions In iron-sufficient men, mild intensification of exercise intensity increases both inflammation and erythropoiesis. The net effect is to decrease hepcidin concentrations and to tend to increase oral iron absorption. This trial was registered at clinicaltrials.gov as NCT01730521.


2004 ◽  
Vol 74 (6) ◽  
pp. 435-443 ◽  
Author(s):  
Hertrampf ◽  
Olivares

Iron amino acid chelates, such as iron glycinate chelates, have been developed to be used as food fortificants and therapeutic agents in the prevention and treatment of iron deficiency anemia. Ferrous bis-glycine chelate (FeBC), ferric tris-glycine chelate, ferric glycinate, and ferrous bis-glycinate hydrochloride are available commercially. FeBC is the most studied and used form. Iron absorption from FeBC is affected by enhancers and inhibitors of iron absorption, but to a lesser extent than ferrous sulfate. Its absorption is regulated by iron stores. FeBC is better absorbed from milk, wheat, whole maize flour, and precooked corn flour than is ferrous sulfate. Supplementation trials have demonstrated that FeBC is efficacious in treating iron deficiency anemia. Consumption of FeBC-fortified liquid milk, dairy products, wheat rolls, and multi-nutrient beverages is associated with an improvement of iron status. The main limitations to the widespread use of FeBC in national fortification programs are the cost and the potential for promoting organoleptic changes in some food matrices. Additional research is required to establish the bioavailability of FeBC in different food matrices. Other amino acid chelates should also be evaluated. Finally there is an urgent need for more rigorous efficacy trials designed to define the relative merits of amino acid chelates when compared with bioavailable iron salts such as ferrous sulfate and ferrous fumarate and to determine appropriate fortification levels


Author(s):  
Joanna Gajewska ◽  
Jadwiga Ambroszkiewicz ◽  
Witold Klemarczyk ◽  
Ewa Głąb-Jabłońska ◽  
Halina Weker ◽  
...  

Iron metabolism may be disrupted in obesity, therefore, the present study assessed the iron status, especially ferroportin and hepcidin concentrations, as well as associations between the ferroportin-hepcidin axis and other iron markers in prepubertal obese children. The following were determined: serum ferroportin, hepcidin, ferritin, soluble transferrin receptor (sTfR), iron concentrations and values of hematological parameters as well as the daily dietary intake in 40 obese and 40 normal-weight children. The ferroportin/hepcidin and ferritin/hepcidin ratios were almost two-fold lower in obese children (p = 0.001; p = 0.026, respectively). Similar iron concentrations (13.2 vs. 15.2 µmol/L, p = 0.324), the sTfR/ferritin index (0.033 vs. 0.041, p = 0.384) and values of hematological parameters were found in obese and control groups, respectively. Iron daily intake in the obese children examined was consistent with recommendations. In this group, the ferroportin/hepcidin ratio positively correlated with energy intake (p = 0.012), dietary iron (p = 0.003) and vitamin B12 (p = 0.024). In the multivariate regression model an association between the ferroportin/hepcidin ratio and the sTfR/ferritin index in obese children (β = 0.399, p = 0.017) was found. These associations did not exist in the controls. The results obtained suggest that in obese children with sufficient iron intake, the altered ferroportin-hepcidin axis may occur without signs of iron deficiency or iron deficiency anemia. The role of other micronutrients, besides dietary iron, may also be considered in the iron status of these children.


Blood ◽  
1963 ◽  
Vol 22 (4) ◽  
pp. 406-415 ◽  
Author(s):  
MARCEL E. CONRAD ◽  
WILLIAM H. CROSBY ◽  
Betty Merrill

Abstract Radioautographic studies provide evidence to support a concept of the mechanism whereby the small intestine controls absorption of iron. Three different states of the body’s iron stores have been considered in this regard: iron excess, iron deficiency and normal iron repletion. As the columnar epithelial cells of the duodenal villi are formed they incorporate a portion of intrinsic iron from the body’s iron store, the amount depending upon the body’s requirement for new iron. It is predicated that with iron excess the iron-receptor mechanism in these cells is saturated with intrinsic iron; this then prevents the cell from accepting dietary iron. In the normal state of iron repletion the receptor mechanism remains partly unsaturated, allowing small amounts of dietary iron to enter the cell. Part of this proceeds into the body to satisfy any metabolic requirement for iron. Part is retained in the mucosal epithelial cells to complete the saturation of the iron-receptor mechanism. This bound iron is subsequently lost when the epithelial cells are sloughed at the end of their life cycle. In iron deficiency it is postulated that the receptor system is inactive or diminished so that entry of dietary iron into the body is relatively uninhibited.


2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Korry J. Hintze ◽  
James P. McClung

Iron status affects cognitive and physical performance in humans. Recent evidence indicates that iron balance is a tightly regulated process affected by a series of factors other than diet, to include hypoxia. Hypoxia has profound effects on iron absorption and results in increased iron acquisition and erythropoiesis when humans move from sea level to altitude. The effects of hypoxia on iron balance have been attributed to hepcidin, a central regulator of iron homeostasis. This paper will focus on the molecular mechanisms by which hypoxia affects hepcidin expression, to include a review of the hypoxia inducible factor (HIF)/hypoxia response element (HRE) system, as well as recent evidence indicating that localized adipose hypoxia due to obesity may affect hepcidin signaling and organismal iron metabolism.


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