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Iron Absorption (iron + absorption)

Distribution by Scientific Domains

Medical Sciences	86%

Kinds of Iron Absorption

intestinal iron absorption

Selected Abstracts

Food Iron Absorption and Its Importance for the Design of Food Fortification Strategies

NUTRITION REVIEWS, Issue 2002
Sean Lynch M.D.
First page of article [source]

How to Ensure Adequate Iron Absorption from Iron-fortified Food

NUTRITION REVIEWS, Issue 2002
Richard Hurrell Ph.D.
First page of article [source]

The Effects of Inhibition of Haem Biosynthesis by Griseofulvin on Intestinal Iron Absorption

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 4 2004
Abas H. Laftah
Urinary 5-aminolaevulinic acid levels were increased within 24 hr of feeding mice with griseofulvin diet (2.5% w/w), with more marked increases seen after 3,7 days. Urinary porphobilinogen levels also showed a similar trend. In vivo intestinal iron absorption was significantly reduced (P<0.05) in experimental mice, mainly due to reduction in the transfer of 59Fe from the enterocytes to the portal circulation. In vitro studies using isolated duodenal fragments also exhibited marked decreases in both iron uptake and Fe (III) reduction. Changes in mucosal Divalent Metal Transporter 1 (DMT-1), Dcytb and Ireg1 (iron regulated protein 1) mRNA levels paralleled the changes in iron absorption. The reduction in iron absorption after griseofulvin treatment was normalised when mice were simultaneously injected with haem-arginate. These data support the hypothesis that intermediates in haem biosynthesis, particularly 5-aminolaevulinic acid, regulate intestinal iron absorption. [source]

Iron Absorption: Biochemical and Molecular Insights into the Importance of Iron Species for Intestinal Uptake

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2002
Piero Cremonesi
Redox chemistry of iron is particularly important in iron metabolism, both as a potential source of toxic intermediates and as an essential requirement for efficient iron transport. The initial step in iron absorption (uptake from lumen to mucosa) is particularly important and several pathways involving Fe(III) reduction or transport and Fe(II) transport have been identified. Novel genes associated with iron uptake include Dcytb, a putative iron-regulated reductase and DMT1, a Fe(II) carrier in the brush border membrane. Other mechanisms may also operate, however. We review the recent findings and apply this to understanding the absorption of Fe(III) pharmaceuticals. [source]

Effects of Alcohol Consumption on Iron Metabolism in Mice with Hemochromatosis Mutations

ALCOHOLISM, Issue 1 2007
Jonathan M. Flanagan
Background: Alcoholic liver disease is associated with increased hepatic iron accumulation. The liver-derived peptide hepcidin is the central regulator of iron homeostasis and recent animal studies have demonstrated that exposure to alcohol reduces hepcidin expression. This down-regulation of hepcidin in vivo implies that disturbed iron sensing may contribute to the hepatosiderosis seen in alcoholic liver disease. Alcohol intake is also a major factor in expression of the hemochromatosis phenotype in patients homozygous for the C282Y mutation of the HFE gene. Methods: To assess the effect of alcohol in mice with iron overload, alcohol was administered to mice with disrupted Hfe and IL-6 genes and Tfr2 mutant mice and their respective 129x1/SvJ, C57BL/6J, and AKR/J wild-type congenic strains. Iron absorption, serum iron levels, and hepcidin expression levels were then measured in these mice compared with water-treated control mice. Results: Alcohol was shown to have a strain-specific effect in 129x1/SvJ mice, with treated 129x1/SvJ mice showing a significant increase in iron absorption, serum iron levels, and a corresponding decrease in hepcidin expression. C57BL/6J and AKR/J strain mice showed no effect from alcohol treatment. 129x1/SvJ mice heterozygous or homozygous for the Hfe knockout had a diminished response to alcohol. All 3 strains were shown to have high blood alcohol levels. Conclusions: The effect of alcohol on iron homeostasis is dependent on the genetic background in mice. In an alcohol-susceptible strain, mutation of the Hfe gene diminished the response of the measured iron indices to alcohol treatment. This indicates that either maximal suppression of hepcidin levels had already occurred as a result of the Hfe mutation or that Hfe was a component of the pathway utilized by EtOH in suppressing hepcidin production and increasing iron absorption. [source]

Effect of transition metal ions (cobalt and nickel chlorides) on intestinal iron absorption

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 9 2004
G. O. Latunde-Dada
Abstract Background, Haem biosynthesis may regulate intestinal iron absorption through changes in cellular levels of ,-aminolaevulinic acid (ALA), haem and perhaps other intermediates. CoCl2 and NiCl2 are activators of haem oxygenase, the rate-limiting enzyme in haem catabolism. Co2+ and Ni2+ may also regulate and increase iron absorption through a mechanism that simulates hypoxic conditions in the tissues. Design, We assayed intestinal iron absorption in mice dosed with CoCl2 or NiCl2. The effects of these metal ions on splenic and hepatic levels of ALA synthase and dehydratase as well as urinary levels of ALA and phosphobilinogen were also assayed. Results, While Co2+ enhanced iron absorption when administered to mice at doses of 65, 125 and 250 µmoles kg,1 body weight, Ni2+ was effective only at the highest dose. Ni2+ but not Co2+ at the highest dose reduced urinary ALA in the treated mice. Both metals ions increased splenic expression of haem oxygenase 1 and iron regulated protein 1, proteins involved, respectively, in haem degradation and iron efflux. Co2+ induced erythropoietin expression. Conclusions, The data suggest that while the effect of Ni2+ on iron absorption could be explained by effects on ALA, the effect of Co2+ may not be explained simply by changes in haem metabolism; therefore, effects mediated by alterations of specific haemoproteins by mechanisms that simulate tissue hypoxia could be important. [source]

Iron status in Danish men 1984,94: a cohort comparison of changes in iron stores and the prevalence of iron deficiency and iron overload

EUROPEAN JOURNAL OF HAEMATOLOGY, Issue 6 2002
Nils Milman
Abstract:,Background and objectives : From 1954 to 1987, flour in Denmark was fortified with 30 mg carbonyl iron per kg. This mandatory fortification was abolished in 1987. The aim of this study was to compare iron status in Danish men before and after abolition of iron fortification. Methods : Iron status (serum ferritin, haemoglobin), was assessed in population surveys in Copenhagen County during 1983,84 comprising 1324 Caucasian men (1024 non-blood-donors, 300 blood donors) and in 1993,94 comprising 1288 Caucasian men (1103 non-blood-donors, 185 donors), equally distributed in age cohorts of 40, 50, 60 and 70 yr. Results : In the 1984 survey median serum ferritin values in the four age cohorts in non-blood-donors were 136, 141, 133 and 111 µg/L, and in the 1994 survey 177, 173, 186 and 148 µg L ,1 , respectively. The difference was significant in all age groups ( P <0.001). There was no significant difference between the two surveys concerning the prevalence of small iron stores (ferritin 16,32 µg L ,1 ), depleted iron stores (ferritin <16 µg L ,1 ) or iron-deficiency anaemia (ferritin <13 µg L ,1 and Hb <5th percentile for iron-replete men). However, from 1984 to 1994, the prevalence of iron overload (ferritin >300 µg L ,1 ) increased from 11.3% to 18.9% ( P <0.0001). During the study period there was an increase in body mass index ( P <0.0001), alcohol consumption ( P <0.03) and use of non-steroid anti-inflammatory drugs (NSAID) ( P <0.0001), and a decrease in the use of vitamin,mineral supplements ( P <0.04) and in the prevalence of tobacco smoking ( P <0.0001). In contrast, median ferritin in blood donors showed a significant fall from 1984 to 1994 (103 vs. 74 µg L ,1 , P <0.02). Conclusion : Abolition of iron fortification reduced the iron content of the Danish diet by an average of 0.24 mg MJ ,1 , and the median dietary iron intake in men from 17 to 12 mg d ,1 . From 1984 to 1994, body iron stores and the prevalence of iron overload in Danish men increased significantly, despite the abolition of food iron fortification. The reason appears to be changes in dietary habits, with a lower consumption of dairy products and eggs, which inhibit iron absorption, and a higher consumption of alcohol, meat, and poultry, containing haem iron and enhancing iron absorption. The high prevalence of iron overload in men may constitute a health risk. [source]

Impaired intestinal iron absorption in Crohn's disease correlates with disease activity and markers of inflammation

INFLAMMATORY BOWEL DISEASES, Issue 12 2006
Gaith Semrin MD
Abstract Background: Anemia in patients with Crohn's disease (CD) is a common problem of multifactorial origin, including blood loss, malabsorption of iron, and anemia of inflammation. Anemia of inflammation is caused by the effects of inflammatory cytokines [predominantly interleukin-6 (IL-6)] on iron transport in enterocytes and macrophages. We sought to elucidate alterations in iron absorption in pediatric patients with active and inactive CD. Methods: Nineteen subjects with CD (8 female, 11 male patients) were recruited between April 2003 and June 2004. After an overnight fast, serum iron and hemoglobin levels, serum markers of inflammation [IL-6, C-reactive protein (CRP), and erythrocyte sedimentation rate], and a urine sample for hepcidin assay were obtained at 8 am. Ferrous sulfate (1 mg/kg) was administered orally, followed by determination of serum iron concentrations hourly for 4 hours after the ingestion of iron. An area under the curve for iron absorption was calculated for each patient data set. Results: There was a strong inverse correlation between the area under the curve and IL-6 (P = 0.002) and area under the curve and CRP levels (P = 0.04). Similarly, the difference between baseline and 2-hour serum iron level (,[Fe]2hr) correlated with IL-6 (P = 0.008) and CRP (P = 0.045). When cutoff values for IL-6 (>5 pg/mL) and CRP (>1.0 mg/dL) were used, urine hepcidin levels also positively correlated with IL-6 and CRP levels (P = 0.003 and 0.007, respectively). Conclusions: Subjects with active CD have impaired oral iron absorption and elevated IL-6 levels compared with subjects with inactive disease. These findings suggest that oral iron may be of limited benefit to these patients. Future study is needed to define the molecular basis for impaired iron absorption. [source]

ORIGINAL ARTICLE: Pro-hepcidin and iron metabolism parameters in multi-time blood donors

INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 5 2010
J. BOINSKA
Summary A high number of blood donations may cause iron depletion. The pathophysiology behind this process may involve hepcidin, a recently discovered peptide that acts by inhibiting iron absorption and promoting iron retention in reticuloendothelial macrophages. The aim of this study was to determine serum pro-hepcidin levels and iron metabolism parameters in multi-time blood donors. The study group consisted of 132 multi-time male blood donors and 25 healthy male volunteers (nondonors). Complete blood cell count and iron status including serum iron, ferritin, soluble transferrin receptor (sTfR), total iron binding capacity (TIBC), unsaturated iron binding capacity (UIBC), erythropoietin and pro-hepcidin (ELISA) were assessed. In blood donors, ferritin level drops markedly in relation to donation frequency (P < 0.001). In contrast, TIBC and UIBC levels increase progressively corresponding to annual donation frequency. Pro-hepcidin concentration increases significantly with the number of donations per year (P = 0.0290). In blood donors having donated blood with the highest frequency per year, pro-hepcidin levels were positively correlated with haemoglobin (R = 0.31, P < 0.05) and negatively with sTfR (R = ,0.31, P < 0.05). Pro-hepcidin levels increase in relation to blood donation frequency per year. Longitudinal studies focusing on changes in serum hepcidin levels are required to address the question whether hepcidin may contribute to iron metabolism disturbances in multi-times blood donors. [source]

Prebiotics and Iron Bioavailability,Is There a Connection?

JOURNAL OF FOOD SCIENCE, Issue 5 2005
Chi Kong Yeung
ABSTRACT: Poor bioavailability of dietary iron, especially from diets rich in cereals and legumes, is a major factor contributing to the high prevalence of nutritional iron deficiency in developing countries. Dietary modification to increase intake of components that promote iron absorption from low-bioavailability meals is an effective strategy for combating nutritional iron deficiency. Prebiotics are nondigestible oligosaccharides that selectively stimulate the growth and activity of specific species of bacteria in the colon with benefits to human health. Common prebiotics such as inulin and fructooligosaccharides occur naturally in a wide variety of plant-based foods and have recently been suggested to have an enhancing effect on iron absorption. The hypothesis that prebiotics enhance iron absorption is biologically plausible because fermentation of prebiotics by natural microflora present in the colon may decrease the pH of the luminal content, promote reduction of Fe(III) to Fe(II), stimulate proliferation of epithelial cells to expand the absorptive surface area, and potentially stimulate expression of mineral-transport proteins in epithelial cells. However, data available in the literature characterizing the enhancing properties of prebiotics on iron absorption are inconsistent, and mechanisms of actions involved are poorly understood. The notion that the colon can function as a significant site of iron absorption in response to stimulation by prebiotics, and the effect of long-term exposure to prebiotics on the iron status of iron-deficient subjects remain to be clarified. This review discusses the functional properties of prebiotics as a promising dietary factor that enhances iron absorption. Keywords: prebiotics, iron, colon, oligosaccharides, inulin [source]

Effects of Alcohol Consumption on Iron Metabolism in Mice with Hemochromatosis Mutations

Use of ferrous fumarate to fortify foods for infants and young children

NUTRITION REVIEWS, Issue 9 2010
Richard Hurrell
Ferrous fumarate is currently recommended for use in the fortification of foods for infants and young children. This recommendation is based on the compound's good sensory properties and on results from isotope studies in adults that reported similar iron absorption values for ferrous fumarate and ferrous sulphate (relative bioavailability [RBV] of ferrous fumarate, 100). However, later isotope studies conducted on both iron-replete and iron-deficient young children found that iron absorption from ferrous fumarate was only about 30% of that achieved from ferrous sulphate (RBV, 30). The reasons for the differences observed in adults compared with children are unclear but could be related to the following factors: lower iron status in children resulting in greater iron absorption via upregulation from ferrous sulphate but not from ferrous fumarate; reduced gastric acid secretion in children leading to retarded dissolution of ferrous fumarate; or an influence of added ascorbic acid on RBV. Ferrous fumarate-fortified complementary foods have been demonstrated to improve iron status in iron-deficient infants and, more recently, to prevent iron deficiency equally as well as ferrous sulphate in iron-replete infants. However, current evidence indicates that iron-deficient infants and young children may absorb iron from ferrous fumarate less well than iron from ferrous sulfate and that, for equivalent efficacy, complementary foods targeted at such infants and young children should contain more iron in the form of fumarate. [source]

Patterns of hepatic iron distribution in patients with chronically transfused thalassemia and sickle cell disease,

AMERICAN JOURNAL OF HEMATOLOGY, Issue 8 2009
Nilesh R. Ghugre
Patients with sickle cell disease (SCD) appear to be at lower risk of endocrinopathies and cardiac dysfunction than those with thalassemia major (TM). Circulating redox active iron is lower in these patients, possibly due to increased systemic inflammation and circulating cytokines. Hepcidin synthesis is upregulated during chronic inflammation, reducing intestinal iron absorption and promoting retention of iron in the reticuloendothelial cells. Hence, we hypothesized that livers of patients with SCD would exhibit greater iron deposition in sinusoidal spaces relative to hepatocytes and less in portal tracts when compared to patients with TM. To test this hypothesis, iron scoring analysis was performed on 70 clinically indicated liver biopsy specimens from children and young adults with the two syndromes. Sinusoidal scores were lower in around 1 of 4 patients with TM but the relative iron loading in hepatocytes, and portal tracts was identical in both diseases. Sinusoidal iron burdens saturated at low hepatic iron concentration (HIC) while hepatocyte and portal iron depots increased proportionally to HIC. Liver fibrosis was increased in patients with TM regardless of their chronic hepatitis status. Overall, liver iron distribution was relatively insensitive to differences in disease type and to the presence or absence of hepatitis. Am. J. Hematol., 2009. © 2009 Wiley-Liss, Inc. [source]

Mechanisms of iron loading and toxicity

AMERICAN JOURNAL OF HEMATOLOGY, Issue S12 2007
Gregory J. Anderson
Normal iron homeostasis is a finely balanced system that reflects iron absorption, loss and utilization. The body has no mechanism for the active excretion of iron, so body iron levels are controlled at the point of absorption in the small intestine. Disturbances in this equilibrium, such as those leading to enhanced absorption, can have significant clinical consequences. Continued excessive iron uptake is followed by iron deposition in various tissues, ultimately leading to tissue damage, and possibly end-organ failure. In this review, current concepts in normal iron homeostasis, and iron loading are explained. The clinical consequences as well as the differences between primary and secondary iron loading are also reviewed, and some future research priorities are discussed. Am. J. Hematol., 2007. © 2007 Wiley-Liss, Inc. [source]

The Effects of Inhibition of Haem Biosynthesis by Griseofulvin on Intestinal Iron Absorption

Iron Absorption: Biochemical and Molecular Insights into the Importance of Iron Species for Intestinal Uptake

Regulatory mechanisms of intestinal iron absorption,Uncovering of a fast-response mechanism based on DMT1 and ferroportin endocytosis

BIOFACTORS, Issue 2 2010
Marco T. Núñez
Abstract Knowledge on the intestinal iron transport process and the regulation of body iron stores has greatly increased during the last decade. The liver, through the sensing of circulating iron, is now recognized as the central organ in this regulation. High iron levels induce the synthesis of hepcidin, which in turn decreases circulating iron by inhibiting its recycling from macrophages and its absorption at the intestine. Another mechanism for the control of iron absorption by the enterocyte is an active Iron Responsive Element (IRE)/Iron Regulatory Protein (IRP) system. The IRE/IRP system regulates the expression of iron uptake and storage proteins thus regulating iron absorption. Similarly, increasing evidence points to the transcriptional regulation of both divalent metal transporter 1 (DMT1) and ferroportin expression. A new mechanism of regulation related to a phenomenon called the mucosal block is starting to be unveiled. The mucosal block describes the ability of an initial dose of ingested iron to block absorption of a second dose given 2,4 h later. Here, we review the mechanisms involved in the expression of DMT1 and ferroportin, and present recent evidence on the molecular components and cellular processes involved in the mucosal block response. Our studies indicate that mucosal block is a fast-response endocytic mechanism destined to decrease intestinal iron absorption during a high ingest of iron. [source]

Role of interleukin-6 in hypoxic regulation of intestinal iron absorption

BRITISH JOURNAL OF HAEMATOLOGY, Issue 5 2005
Kishor B. Raja
Summary The regulation of intestinal iron absorption is not fully understood. Hepcidin, a liver-produced peptide, has recently been identified as a negative regulator of iron absorption in various conditions associated with altered iron metabolism (e.g. inflammation, anaemia, hypoxia). It is not clear whether these perturbants share a common signalling pathway. In this study, the importance of the cytokine interleukin-6 (IL-6) was investigated in the hypoxic mouse model. Hypoxia was associated with increased levels of circulating IL-6, decreased liver hepcidin mRNA and increased iron absorption (especially MT). A significant positive correlation existed between the total iron uptake and IL-6 levels in circulation. IL-6 per se, though inducing hepcidin mRNA, failed to affect basal iron absorption. The adaptive response to absorption following the hypoxic exposure was, however, more prominent if mice had been treated concurrently with IL-6. This enhancement in absorption occurred even though hepcidin mRNA was not significantly changed. Similar prominent responses were seen with both human and mouse IL-6. Anti-IL-6 antiserum normalised iron absorption in mice exposed to hypoxia, because of a reduction in the MT. These data indicate that IL-6 can influence iron absorption (especially MT) during the hypoxic exposure, but via a mechanism independent of hepcidin. [source]