Duodenal nonheme iron content correlates with iron stores in mice, but the relationship is altered by Hfe gene knock-out

Blood ◽  
2003 ◽  
Vol 101 (8) ◽  
pp. 3316-3318 ◽  
Author(s):  
Robert J. Simpson ◽  
Edward S. Debnam ◽  
Abas H. Laftah ◽  
Nita Solanky ◽  
Nick Beaumont ◽  
...  
Keyword(s):  
Iron Content ◽  
Iron Absorption ◽  
Hereditary Hemochromatosis ◽  
Iron Concentration ◽  
Nonheme Iron ◽  
Hfe Gene ◽  
Liver Iron ◽  
Knock Out ◽  
Iron Stores ◽  
Knock Out Mice

Abstract Hereditary hemochromatosis is a common iron-loading disorder found in populations of European descent. It has been proposed that mutations causing loss of function of HFE gene result in reduced iron incorporation into immature duodenal crypt cells. These cells then overexpress genes for iron absorption, leading to inappropriate cellular iron balance, a persistent iron deficiency of the duodenal mucosa, and increased iron absorption. The objective was to measure duodenal iron content in Hfe knock-out mice to test whether the mutation causes a persistent decrease in enterocyte iron concentration. In both normal and Hfe knock-out mice, duodenal nonheme iron content was found to correlate with liver iron stores (P < .001, r = 0.643 and 0.551, respectively), and this effect did not depend on dietary iron levels. However, duodenal iron content was reduced in Hfe knock-out mice for any given content of liver iron stores (P < .001).

Combination of Tmprss6-ASO and the Iron Chelator Deferiprone Improves Erythropoiesis and Reduces Iron Overload in a Mouse Model of Beta-Thalassemia

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 4024-4024
Author(s):  
Carla Casu ◽  
Mariam Aghajan ◽  
Rea Oikonomidau ◽  
Shuling Guo ◽  
Brett P. Monia ◽  
...  
Keyword(s):  
Iron Content ◽  
Research Funding ◽  
Serum Iron ◽  
Iron Absorption ◽  
Iron Concentration ◽  
Iron Chelation ◽  
Iron Chelator ◽  
Liver Iron ◽  
Hepcidin Expression ◽  
Liver Iron Content

Abstract Patients affected by non-transfusion dependent thalassemia (NTDT) do not require chronic blood transfusion for survival. However, transfusion-independence in such patients is not without side effects. Ineffective erythropoiesis (IE), the hallmark of disease, leads to a variety of serious clinical morbidities. In NTDT the master regulator of iron homeostasis, hepcidin, is chronically repressed. Consequently, patients absorb abnormally high levels of iron, which eventually requires iron chelation to prevent the clinical sequelaes associated with iron overload. It has been shown that in mice affected by NTDT (Hbbth3/+), a second-generation antisense oligonucleotide (Tmprss6-ASO) can reduce expression of transmembrane serine protease Tmprss6, the major suppressor of hepcidin expression. This leads to reduction of hemichrome formation in erythroid cells, amelioration of IE and splenomegaly, and increased hemoglobin levels (Guo et al, JCI, 2013). Now we propose the use of Tmprss6-ASO in combination with iron chelators for the treatment of NTDT using Hbbth3/+ mice as a preclinical model. Our hypothesis is that use of chelators will benefit from the positive effect of Tmprss6-ASO on erythropoiesis and iron absorption, further ameliorating organ iron content. To this end, Hbbth3/+ animals were treated with Tmprss6-ASO at 100 mg/kg/week for 6 weeks with or without the iron chelator deferiprone (DFP) at a dose of 1.25 mg/ml. Additional animals were treated with DFP alone. We fed the animals with a commercial or physiological diet, containing 200 or 35 ppm of iron, respectively. We did not observe major differences in the treated animals fed the commercial or physiological iron diet and, for this reason, the data were combined for simplicity. Administration of DFP alone was successful in decreasing organ iron content. Compared to untreated Hbbth3/+ animals, we observed a reduction of 30% and 33% in the liver and spleen, respectively, and no change in the kidney. However, erythropoiesis was not improved (looking at IE, splenomegaly, RBC production and total Hb levels). This was associated with increased serum iron levels (+25%). In Tmprss6-ASO treated Hbbth3/+ animals, we observed an improvement in liver iron content (36% reduction), amelioration of IE, and increased RBC and Hb synthesis (~2 g/dL). Compared to treatment with Tmprss6-ASO alone, combination of DFP with Tmprss6-ASO achieved the same level of suppression of Tmprss6 in the liver (~90%) and reduction of serum iron parameters. This was associated with improvement of IE, decreased reticulocyte counts and splenomegaly, and increased RBC and Hb synthesis (~2 g/dL). While we observed that both Tmprss6-ASO and DFP separately reduced liver iron content to the same extent (~30-36%), combination treatment further reduced iron concentrations in the liver and kidney (69% and 19%, respectively), with no changes in the spleen. Additional analyses are in progress to evaluate the amount of hepcidin in serum as well as expression of erythroferrone, the erythroid regulator of hepcidin. Our first conclusion is that administration of an iron chelator alone is not sufficient to improve erythropoiesis despite that organ iron content is reduced. We speculate that when iron is removed from the liver, hepcidin expression becomes more susceptible to the suppressive effect of IE rather than the enhancing effect of reduced liver organ iron concentration. In addition, the combined effect of iron mobilized from organs and unchanged (or even augmented) iron absorption leads to increased serum iron concentration. As we have shown previously, amelioration of IE in this model requires decreased erythroid iron intake and hemichrome formation. Therefore, iron chelation alone is likely insufficient to improve erythropoiesis. Additional experiments are in progress to further elucidate this mechanism. Our second conclusion is that use of Tmprss6-ASO together with DFP combines the best effects of these two drugs, in particular on erythropoiesis and organ iron content. In animals that received the combined treatment, kidney and liver iron concentrations were further decreased compared to the single treatments. This indicates that Tmprss6-ASO might be extremely helpful in the treatment of NTDT and it could further improve iron related-chelation therapies. Disclosures Casu: Merganser Biotech LLC: Employment; Isis Pharmaceuticals, Inc.: Employment. Aghajan:Isis Pharmaceuticals, Inc.: Employment. Guo:Isis Pharmaceuticals, Inc.: Employment. Monia:Isis Pharmaceuticals, Inc.: Employment. Rivella:bayer: Consultancy, Research Funding; isis Pharmaceuticals, Inc.: Consultancy, Research Funding; merganser Biotech LLC: Consultancy, Research Funding, Stock options , Stock options Other.

scholarly journals Discrepancy between Serum Ferritin and Liver Iron Concentration in a Patient with Hereditary Hemochromatosis – The Value of T2* MRI

2020 ◽  
Vol 13 (2) ◽  
pp. 712-715
Author(s):  
Mustafa A. Al-Tikrity ◽  
Mohamed A. Yassin
Keyword(s):  
Iron Overload ◽  
Serum Ferritin ◽  
Ferritin Level ◽  
Hereditary Hemochromatosis ◽  
Iron Concentration ◽  
Hfe Gene ◽  
Liver Iron Concentration ◽  
C282y Mutation ◽  
Liver Iron ◽  
T2 Mri

Primary hemochromatosis is an inherited disorder, and the homeostatic iron regulator (HFE) gene C282Y mutation is a common cause of hemochromatosis in Europe. We are reporting a case of a 56-year-old female known to have hemochromatosis with the HFE gene C282Y mutation with a serum ferritin level of 482 μg/L who underwent heart and liver T2* MRI which showed no evidence of iron overload – neither in the heart nor in the liver. This indicates that there is a discrepancy between serum ferritin and liver iron concentration by MRI and the superiority of T2* MRI in diagnosis and follow-up of iron overload in patients with hereditary hemochromatosis.

scholarly journals Contributions of β2-microglobulin–dependent molecules and lymphocytes to iron regulation: insights from HfeRag1-/- and β2mRag1-/- double knock-out mice

Blood ◽  
2004 ◽  
Vol 103 (7) ◽  
pp. 2847-2849 ◽  
Author(s):  
Carlos J. Miranda ◽  
Hortence Makui ◽  
Nancy C. Andrews ◽  
Manuela M. Santos
Keyword(s):  
Iron Overload ◽  
Hereditary Hemochromatosis ◽  
Protein S ◽  
Iron Accumulation ◽  
Iron Regulation ◽  
Hfe Gene ◽  
Knock Out ◽  
Β2 Microglobulin ◽  
Knock Out Mice ◽  
Deficient Mice

Abstract Genetic causes of hereditary hemochromatosis (HH) include mutations in the HFE gene, coding for a β2-microglobulin (β2m)-associated major histocompatibility complex class I-like protein. However, iron accumulation in patients with HH can be highly variable. Previously, analysis of β2mRag1-/- double-deficient mice, lacking all β2m-dependent molecules and lymphocytes, demonstrated increased iron accumulation in the pancreas and heart compared with β2m single knock-out mice. To evaluate whether the observed phenotype in β2mRag1-/- mice was due solely to the absence of Hfe or to other β2m-dependent molecules, we generated HfeRag1-/- double-deficient mice. Our studies revealed that introduction of Rag1 deficiency in Hfe knock-out mice leads to heightened iron overload, mainly in the liver, whereas the heart and pancreas are relatively spared compared with β2mRag1-/- mice. These results suggest that other β2m-interacting protein(s) may be involved in iron regulation and that in the absence of functional Hfe molecules lymphocyte numbers may influence iron overload severity. (Blood. 2004;103: 2847-2849)

A New Model for Predicting Venesection Therapy Requirements in Hereditary Hemochromatosis Using Non-Invasive Liver Iron Concentration Measurement.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3596-3596 ◽  
Author(s):  
Timothy G. St. Pierre ◽  
Gary P. Jeffrey ◽  
Enrico Rossi ◽  
Adam J. Fleming ◽  
Wanida Chua-anusorn ◽  
...  
Keyword(s):  
Blood Volume ◽  
Hereditary Hemochromatosis ◽  
Iron Concentration ◽  
Liver Volume ◽  
Newly Diagnosed ◽  
Liver Iron ◽  
Body Iron ◽  
Iron Stores ◽  
Straight Line ◽  
Total Body

Abstract Newly diagnosed hereditary hemochromatosis subjects are treated with venesection therapy in order to reduce body iron stores. Liver iron concentration (LIC) is the most reliable indicator of body iron stores. Proton transverse relaxation rate imaging (FerriScan®) enables a highly specific and sensitive measurement of LIC [St. Pierre TG, Clark PR, Chuaanusorn W, Fleming A, Jeffrey GP, Olynyk JK, Pootrakul P, Robins E, Lindeman R. Blood105 (2005) 855–861]. In this study FerriScan® was used to follow the LIC and liver volume in 7 newly diagnosed homozygous C282Y hereditary hemochromatosis patients. Baseline LIC values ranged from 3.4 to 16.7 mg Fe/g dry tissue. The total number of venesected units of blood required to lower the LIC of each subject to the upper end of the normal range was initially estimated from body mass and LIC [Angelucci, E., Brittenham, G.M., McLaren, C.E. et al. (2000) New Eng. J. Med.343, 327–331]. The LIC of each subject was measured again after approximately half the estimated total number of units of blood had been removed, and a third time near completion of the venesection therapy. For each subject, a straight line was fitted to the LIC versus venesected blood volume data. The coefficient of variation of the differences between the measured LIC values and the fitted lines (a measure of the precision of the LIC measurements) was found to be 7 %. Total body iron stores were measured by extrapolating the straight line fit through the LIC vs venesected blood volume to zero LIC and using a value of 0.473 mg Fe/mL for the blood iron concentration. Total liver iron content was determined by simultaneous measurement of LIC and liver volume with MRI. The data indicated that the higher the LIC at diagnosis, the higher was the fraction, α, of the total body iron store located in the liver. Hence a linear model relating α to LIC is proposed, α = β x LIC + α0. Linear regression was used on the 21 measurements of LIC in the study to find the following optimum model parameters α0 = 0.169 and β = 0.0274 g wet liver/mg Fe. Using these parameters the total blood volume (TBV) to be removed from a patient to bring the LIC down from an initial value (LICi) to a target value (LICf) can be calculated using TBV = [(LICi – LICf) x V]/(β x LICi + α0) where V is the liver volume. Using the 21 measurements in this study a straight line relationship between measured and predicted numbers of units of blood to bring LIC to 1 mg Fe/g dry tissue was found to have slope 0.99 and Pearson’s correlation coefficient of 0.97. The data suggest that simultaneous measurement of LIC and liver volume with MRI (data acquisition time less than 30 minutes) can be used to predict venesection requirements in hereditary hemochromatosis. The measurement of baseline LIC also enables an estimate of the possible visceral or metabolic consequences of the iron burden. For example, in the absence of other complicating factors, a measurement of the LIC multiplied by the age of the subject gives a good predictor of iron induced liver damage [Olynyk, J.K, St. Pierre, T.G., Britton, R.S., Brunt, E.M., and Bacon, B.R. (2005) Am. J. Gastro., 100, 837–841].

Mechanisms Regulating Iron Absorption over a Wide Range of Dietary Iron Content in the Mouse.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3578-3578
Author(s):  
Richard S. Ajioka ◽  
Ryan R. Gillespie ◽  
James P. Kushner
Keyword(s):  
Iron Content ◽  
Iron Absorption ◽  
Iron Concentration ◽  
Hepatic Iron ◽  
Dietary Iron ◽  
Wild Mice ◽  
Transcript Levels ◽  
Hepcidin Expression ◽  
Iron Stores ◽  
Wide Range

Abstract Dietary iron absorption by enterocytes is mediated by a ferrous transporter (DMT1) and possibly a ferric reductase (Cbyrd1). The role of Cbyrd1 is uncertain, as a knockout mouse has no defect in absorption (Gunshin et al. Blood, 2005, June 16, Epub). Transfer of iron to plasma is mediated by ferroportin (FPN). FPN’s residence on the basolateral membrane is regulated by hepcidin (Nemeth et al. Science 2004, 306:2090–3). Iron absorption responds to erythropoiesis, hypoxia and iron stores. A dietary iron content of 120 mg/kg consumed will maintain hepatic iron stores near that of mice found in the wild. Mice will grow and breed given diets containing 35 mg/kg. Commercial mouse chow iron content ranges from 200–350 mg/kg. We studied the effects of diets containing 2, 35, 120, 350 and 2000 mg iron/kg on iron absorption, liver and spleen iron content and transcriptional levels of DMT1, FPN and hepcidin in A/J mice. Mice were weaned at 3 weeks of age and groups of 8 animals were placed on one of the 5 diets for 4 weeks. No differences between groups were noted in hematocrit, hemoglobin and MCV. Mean hepatic iron content was 52.7 ±3.7 ug/g (wet wt) in mice fed the 2 mg/kg diet. Mean hepatic iron content was 560 ±23.7 ug/g in mice fed the 2000 mg/kg diet. There was no difference in hepatic iron content in mice fed intermediate iron diets (35–350 mg/kg). Mean hepatic iron concentration in these groups was 110 ±3 ug/g. Mean spleen iron content was 132 ±12.2 ug/g (wet wt) in mice maintained on 2 mg/kg. Mean spleen iron content was 598 ±49 ug/g in mice fed the 2000 mg/kg diet. There was no difference in spleen iron content in mice maintained on intermediate iron diets (mean 359 ±10 ug/g). These data indicate that mice maintain constant levels of hepatic and splenic iron over a ten-fold range in dietary iron content. Iron absorption was measured as percent of a measured dose of 59Fe (5 ug total) remaining in the carcass (minus the GI tract) 24 h after administration by gavage. Absorption was inversely proportional to dietary iron content. Mean absorption was 86% ±4 in the group on the 2 mg/kg diet, 42% ±3 on the 35 mg/kg diet, 26% ±7 on the 120 mg/kg diet, 19% ±4 on the 350 mg/kg diet and 6% ±1 on the 2000 mg/kg diet. Transcript levels of hepcidin, DMT1 and FPN were measured by real-time PCR and normalized to beta actin mRNA. Liver hepcidin expression was 20-fold greater in mice on the 2000 mg/kg diet than in mice on the 2 mg/kg diet (3900 ±1021 copies/actin copy vs. 198 ±47). Hepcidin expression did not differ in mice on intermediate diets (745 ±147 copies). Enterocytes were isolated from everted gut explants by elution in EDTA. Transcript levels of enterocyte DMT1 and FPN were 4566 ±SEM and 236 ±SEM copies respectively in mice on the 2 mg/kg diet. No detectable transcripts were found in mice on the 2000 mg/kg diet. Enterocyte transcript levels for DMT1 and FPN were no different in groups on intermediate iron diets (17 ±2 copies and 20 ±9 copies respectively). These data indicate that tissue iron content, hepcidin, DMT1 and FPN remain constant over a ten-fold range in dietary iron and only vary at extremes, while iron absorption is inversely proportional to dietary iron. The data also suggest that dietary iron, within defined limits, regulates iron absorption by a mechanism intrinsic to the enterocyte.

scholarly journals Contribution of Hfe expression in macrophages to the regulation of hepatic hepcidin levels and iron loading

Blood ◽  
2005 ◽  
Vol 106 (6) ◽  
pp. 2189-2195 ◽  
Author(s):  
Hortence Makui ◽  
Ricardo J. Soares ◽  
Wenlei Jiang ◽  
Marco Constante ◽  
Manuela M. Santos
Keyword(s):  
Bone Marrow ◽  
Iron Absorption ◽  
Hereditary Hemochromatosis ◽  
Peptide Hormone ◽  
Hfe Gene ◽  
Mrna Levels ◽  
Iron Loading ◽  
Liver Iron ◽  
Hepcidin Expression ◽  
Hepcidin Mrna

Abstract Hereditary hemochromatosis (HH), an iron overload disease associated with mutations in the HFE gene, is characterized by increased intestinal iron absorption and consequent deposition of excess iron, primarily in the liver. Patients with HH and Hfe-deficient (Hfe-/-) mice manifest inappropriate expression of the iron absorption regulator hepcidin, a peptide hormone produced by the liver in response to iron loading. In this study, we investigated the contribution of Hfe expression in macrophages to the regulation of liver hepcidin levels and iron loading. We used bone marrow transplantation to generate wild-type (wt) and Hfe-/- mice chimeric for macrophage Hfe gene expression. Reconstitution of Hfe-deficient mice with wt bone marrow resulted in augmented capacity of the spleen to store iron and in significantly decreased liver iron loading, accompanied by a significant increase of hepatic hepcidin mRNA levels. Conversely, wt mice reconstituted with Hfe-deficient bone marrow had a diminished capacity to store iron in the spleen but no significant alterations of liver iron stores or hepcidin mRNA levels. Our results suggest that macrophage Hfe participates in the regulation of splenic and liver iron concentrations and liver hepcidin expression. (Blood. 2005;106:2189-2195)

scholarly journals Hfe Gene Knock-Out in a Mouse Model of Hereditary Hemochromatosis Affects Bodily Iron Isotope Compositions

2021 ◽  
Vol 8 ◽  
Author(s):  
Emmanuelle Albalat ◽  
Thibault Cavey ◽  
Patricia Leroyer ◽  
Martine Ropert ◽  
Vincent Balter ◽  
...  
Keyword(s):  
Iron Overload ◽  
Iron Metabolism ◽  
Whole Blood ◽  
Isotope Composition ◽  
Hereditary Hemochromatosis ◽  
Iron Concentration ◽  
Hfe Gene ◽  
Iron Isotope ◽  
Heavy Isotope ◽  
Knock Out

Hereditary hemochromatosis is a genetic iron overload disease related to a mutation within the HFE gene that controls the expression of hepcidin, the master regulator of systemic iron metabolism. The natural stable iron isotope composition in whole blood of control subjects is different from that of hemochromatosis patients and is sensitive to the amount of total iron removed by the phlebotomy treatment. The use of stable isotopes to unravel the pathological mechanisms of iron overload diseases is promising but hampered by the lack of data in organs involved in the iron metabolism. Here, we use Hfe−/− mice, a model of hereditary hemochromatosis, to study the impact of the knock-out on iron isotope compositions of erythrocytes, spleen and liver. Iron concentration increases in liver and red blood cells of Hfe−/− mice compared to controls. The iron stable isotope composition also increases in liver and erythrocytes, consistent with a preferential accumulation of iron heavy isotopes in Hfe−/− mice. In contrast, no difference in the iron concentration nor isotope composition is observed in spleen of Hfe−/− and control mice. Our results in mice suggest that the observed increase of whole blood isotope composition in hemochromatosis human patients does not originate from, but is aggravated by, bloodletting. The subsequent rapid increase of whole blood iron isotope composition of treated hemochromatosis patients is rather due to the release of hepatic heavy isotope-enriched iron than augmented iron dietary absorption. Further research is required to uncover the iron light isotope component that needs to balance the accumulation of hepatic iron heavy isotope, and to better understand the iron isotope fractionation associated to metabolism dysregulation during hereditary hemochromatosis.

Effect of transfusional iron intake on response to chelation therapy in β-thalassemia major

Blood ◽  
2008 ◽  
Vol 111 (2) ◽  
pp. 583-587 ◽  
Author(s):  
Alan R. Cohen ◽  
Ekkehard Glimm ◽  
John B. Porter
Keyword(s):  
Chelation Therapy ◽  
Iron Concentration ◽  
Chelating Agent ◽  
Thalassemia Major ◽  
Phase Iii ◽  
Iron Loading ◽  
Iron Intake ◽  
Liver Iron ◽  
Iron Stores ◽  
Using Data

The success of chelation therapy in controlling iron overload in patients with thalassemia major is highly variable and may partly depend on the rate of transfusional iron loading. Using data from the 1-year phase III study of deferasirox, including volumes of transfused red blood cells and changes in liver iron concentration (LIC) in 541 patients, the effect of iron loading on achieving neutral or negative iron balance was assessed in patients receiving different doses of deferasirox and the comparator deferoxamine. After dose adjustment, reductions in LIC after 1 year of deferasirox or deferoxamine therapy correlated with transfusional iron intake. At a deferasirox dose of 20 mg/kg per day, neutral or negative iron balance was achieved in 46% and 75% of patients with the highest and lowest transfusional iron intake, respectively; 30 mg/kg per day produced successful control of iron stores in 96% of patients with a low rate of transfusional iron intake. Splenectomized patients had lower transfusional iron intake and greater reductions in iron stores than patients with intact spleens. Transfusional iron intake should be monitored on an ongoing basis in thalassemia major patients, and the rate of transfusional iron loading should be considered when choosing the appropriate dose of an iron-chelating agent. This study is registered at http://clinicaltrials.gov as NCT00061750.

The effect of deferasirox on cardiac iron in thalassemia major: impact of total body iron stores

Blood ◽  
2010 ◽  
Vol 116 (4) ◽  
pp. 537-543 ◽  
Author(s):  
John C. Wood ◽  
Barinder P. Kang ◽  
Alexis Thompson ◽  
Patricia Giardina ◽  
Paul Harmatz ◽  
...  
Keyword(s):  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Iron Concentration ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Liver Iron ◽  
Ventricular Ejection Fraction ◽  
Iron Stores ◽  
Cardiac Iron

AbstractWe present results from a prospective, multicenter, open-label, single-arm study evaluating response of cardiac and liver iron to deferasirox therapy for 18 months. Twenty-eight patients with abnormal T2* and normal left ventricular ejection fraction were enrolled from 4 US centers. All patients initially received deferasirox doses of 30 to 40 mg/kg per day. Patients were severely iron overloaded: mean liver iron concentration (LIC) 20.3 mg Fe/g dry weight, serum ferritin 4417 ng/mL, and cardiac T2* 8.6 ms. In the intent-to-treat population, 48% reached the primary endpoint (cardiac T2* improvement at 18 months, P = not significant). There were 2 deaths: 1 from congestive heart failure and 1 from sepsis. In the 22 patients completing the trial, LIC and cardiac T2* improvements were 16% (P = .06) and 14% (P = .07), respectively. Cardiac T2* improvement (13 patients) was predicted by initial LIC, final LIC, and percentage LIC change, but not initial cardiac T2*. Cardiac iron improved 24% in patients having LIC in the lower 2 quartiles and worsened 8.7% in patients having LIC in the upper 2 quartiles. Left ventricular ejection fraction was unchanged at all time points. Monotherapy with deferasirox was effective in patients with mild to moderate iron stores but failed to remove cardiac iron in patients with severe hepatic iron burdens. This study was registered at www.clinicaltrials.gov as #NCT00447694.

Mineral absorption of diets containing natural carob fiber compared to cellulose, pectin and various combinations of these fibers Absorción de minerales de dietas que contienen fibra natural de algarrobas comparada con celulosa, pectina y varias combinaciones de estas fibras

2000 ◽  
Vol 6 (6) ◽  
pp. 463-471 ◽  
Author(s):  
M.P. Vaquero ◽  
L. Perez-Olleros ◽  
M. Garcia-Cuevas ◽  
M. Veldhuizen ◽  
B. Ruiz-Roso ◽  
...  
Keyword(s):  
Iron Absorption ◽  
Calcium Absorption ◽  
Iron Concentration ◽  
Liver Iron Concentration ◽  
Liver Iron ◽  
Final Body Weight ◽  
Mineral Absorption ◽  
Apparent Absorption ◽  
Zinc Concentrations ◽  
Calcium Magnesium

The influence of the consumption of natural carob fiber (NCF), an insoluble hypocholesterolemic fiber, as the unique dietary fiber or combined with cellulose (CEL) or pectin (PEC), on mineral bioavailability was studied. Six groups of rats were fed for 10 days diets containing 10% CEL, NCF, PEC or CEL+NCF, CEL+PEC and NCF+PEC mixtures at 50%. Food intake was lower with PEC than NCF and CEL+NCF, but final body weight was unaffected. Fecal weight showed significant differ ences in the following order: CEL, NCF, CEL+NCF > CEL+PEC, NCF+PEC > PEC. Percentage of calcium absorption was higher with CEL+PEC and NCF+PEC compared with the rest of fibers. Mag nesium absorption was also significantly enhanced in these two groups compared to NCF (p < 0.0004). Iron absorption did not show variations. Zinc apparent absorption was reduced by PEC, but the NCF+PEC mixture counterbalanced this effect. Liver iron was significantly lower with NCF+PEC than CEL, and liver iron concentration was significantly lower with NCF+PEC compared to CEL+PEC. Liver zinc was significantly higher with CEL+NCF than PEC while liver zinc concentrations were slightly higher with the former (p = 0.05 compared to NCF). The results indicate that NCF, compared to CEL and PEC, did not decrease the efficiency of calcium, magnesium and iron absorption in rats, while compared to PEC it increased zinc apparent absorption. Moreover, by combining NCF with PEC calcium and magnesium, absorptions enhanced in comparison with NCF alone, which was prob ably a result of the combination of soluble and insoluble fibers.

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