Mammalian Iron Metabolism and Dietary Iron Absorption

2016 ◽  
pp. 247-264 ◽  
Keyword(s):  
Iron Metabolism ◽  
Iron Absorption ◽  
Dietary Iron

scholarly journals Abnormalities of iron metabolism and erythropoiesis in vitamin E- deficient rabbits

Blood ◽  
1978 ◽  
Vol 52 (1) ◽  
pp. 187-195 ◽  
Author(s):  
AC Chou ◽  
GO Jr Broun ◽  
CD Fitch
Keyword(s):  
Skeletal Muscle ◽  
Bone Marrow ◽  
Vitamin E ◽  
Iron Metabolism ◽  
Iron Absorption ◽  
Iron Concentration ◽  
Vitamin E Deficiency ◽  
Deficient Diet ◽  
Plasma Iron ◽  
Erythroid Hyperplasia

Abstract Rabbits fed a vitamin E-deficient diet developed severe muscular dystrophy in 3–4 wk, but they did not become anemic. Nevertheless, reticulocyte counts increased in deficient rabbits (3.2%) compared to control rabbits (0.9%), and erythroid hyperplasia was evident in the bone marrow. Comparing deficient rabbits to controls, the plasma iron concentration was lower (134.4 versus 206.6 microgram/dl); the TIBC was higher (335.9 versus 228.3 microgram/dl); the whole blood protoporphyrin concentration was higher (131.6 versus 81.7 microgram/dl); and the total iron content was lower in spleen (71 versus 153 microgram), higher in skeletal muscle (4956 versus 3054 microgram), and unchanged in bone marrow, liver, and heart. Studies of iron absorption and excretion using 59Fe showed no abnormalities in deficient rabbits. There were abnormalities of ferrokinetics, however. The half-time of disappearance of 59Fe was shorter (100.6 versus 169.4 min), the plasma iron turnover was greater (1.25 versus 0.95 mg/dl blood/day), and the reappearance of 59Fe in circulating erythrocytes at day 9 was greater (77.2% versus 57.2%) in deficient rabbits. Anemia induced by phlebotomy accentuated the abnormal iron metabolism of deficient rabbits, and the animals were unable to correct the anemia. These findings show that vitamin E deficiency in rabbits causes abnormal erythropoiesis associated with abnormal iron metabolism and sequestration of iron in skeletal muscle.

scholarly journals IRON METABOLISM

Blood ◽  
1950 ◽  
Vol 5 (11) ◽  
pp. 983-1008 ◽  
Author(s):  
CLEMENT A. FINCH ◽  
MARK HEGSTED ◽  
THOMAS D. KINNEY ◽  
E. D. THOMAS ◽  
CHARLES E. RATH ◽  
...  
Keyword(s):  
Iron Metabolism ◽  
Serum Iron ◽  
Iron Absorption ◽  
Binding Protein ◽  
The Body ◽  
Iron Binding ◽  
Body Iron ◽  
Iron Administration ◽  
Parenteral Iron ◽  
Iron Binding Protein

Abstract On the basis of experimental and clinical observations and a review of the literature, a concept of the behavior of storage iron in relation to body iron metabolism has been formulated. Storage iron is defined as tissue iron which is available for hemoglobin synthesis when the need arises. This iron is stored intracellularly in protein complex as ferritin and hemosiderin. It would appear that wherever the cell is functionally intact, such iron is available for general body needs. Iron is transported by a globulin of the serum to and from the various tissues of the body to satisfy their metabolism. Surplus iron carried by this iron-binding protein is deposited chiefly in the liver. Storage iron may be increased in two ways. The first mechanism results from the inability of the body to excrete significant amounts of iron. Because of this, any decrease in circulating red cell iron (any anemia other than blood loss or iron deficiency anemia) is accompanied by a shift of iron to the tissue compartment. The total amount of body iron remains constant and is merely redistributed. This is to be contrasted with the absolute increase in body iron and enlarged iron stores which follow excessive iron absorption or parenteral iron administration. Enlarged iron stores in either instance may be evaluated by examination of sternal marrow or determination of the serum iron and saturation of the iron binding protein In states of iron excess, differences in initial distribution are observed, depending on the route of administration and type of iron compound employed. Iron absorbed from the gastro-intestinal tract and soluble iron salts injected in small amounts are transported by the iron-binding protein of the serum and stored predominantly in the liver. Colloidal iron given intravenously is taken up by the reticulo-endothelial tissue. Erythrocytes appear to localize in greatest concentration in the spleen, while greater amounts of hemoglobin iron are found in the renal parenchyma. These latter differences in distribution reflect the capacity of various body tissues to assimilate different iron compounds, which while present in the plasma are not carried by the iron-binding protein. Over a period of time an internal redistribution of iron from these various sites occurs through the serum iron compartment. The liver becomes progressively loaded with iron. When the capacity of the liver to store iron is exceeded, the serum iron increases and secondary tissue receptors begin to fill with iron. That iron in large amounts is toxic to tissues is suggested by the occurrence of fibrosis in the organs most heavily laden with iron. This sequence of events, whether following excessive iron absorption or parenteral iron administration is believed to be responsible for the clinical and pathologic picture of hemochromatosis.

scholarly journals Intestinal Mucosal Mechanisms Controlling Iron Absorption

Blood ◽  
1963 ◽  
Vol 22 (4) ◽  
pp. 406-415 ◽  
Author(s):  
MARCEL E. CONRAD ◽  
WILLIAM H. CROSBY ◽  
Betty Merrill
Keyword(s):  
Iron Deficiency ◽  
Epithelial Cells ◽  
Iron Absorption ◽  
The Body ◽  
Iron Store ◽  
Dietary Iron ◽  
Receptor System ◽  
Excess Iron ◽  
Metabolic Requirement ◽  
Iron Receptor

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.

scholarly journals Hookworm Anemia: Iron Metabolism and Erythrokinetics

Blood ◽  
1961 ◽  
Vol 18 (1) ◽  
pp. 61-72 ◽  
Author(s):  
MIGUEL LAYRISSE ◽  
ALFREDO PAZ ◽  
NORMA BLUMENFELD ◽  
MARCEL ROCHE ◽  
Iris Dugarte ◽  
...  
Keyword(s):  
Iron Metabolism ◽  
Iron Absorption ◽  
Binding Capacity ◽  
Fecal Excretion ◽  
Red Cell ◽  
Hookworm Infection ◽  
Cell Production ◽  
Plasma Iron ◽  
Deficiency Type ◽  
Iron Binding Capacity

Abstract Iron metabolism, balance of red cell production and destruction and iron absorption from hemoglobin were determined in 11 patients with heavy hookworm infection and severe anemia. The plasma iron, total iron binding capacity, bone marrow hemosiderin and plasma Fe59 clearance are in agreement with the idea that the anemia associated with hookworm infection is of the iron deficiency type. The rate of red cell production measured by the E/M ratio, absolute reticulocyte count and plasma iron turnover showed an increase to about twice normal, while the rate of destruction estimated by the T ½ erythrocyte survival showed a destruction about 5 times normal. This unbalance between production and destruction could explain the severity of the anemia. The increase of fecal urobilinogen output to twice normal was interpreted as due to the metabolism of the hemoglobin lost into the intestine rather than to an increase of hemolysis. The estimation of fecal blood loss in the patients whose red cells were tagged with Cr51 and Fe59, showed that the radioactivity counted with Fe59 was only about 63 per cent of the radioactivity counted with Cr51. This difference was interpreted as due to iron absorption from the hemoglobin lost into the intestine. The mean daily fecal excretion of iron reaches 4.7 mg. Since the iron metabolism in these patients is in equilibrium, we have concluded that the iron loss is replaced by the iron from food; this is in addition to the 3 mg. hemoglobin iron which is reabsorbed from the blood lost into the gut.

scholarly journals Iron age: novel targets for iron overload

Hematology ◽  
2014 ◽  
Vol 2014 (1) ◽  
pp. 216-221 ◽  
Author(s):  
Carla Casu ◽  
Stefano Rivella
Keyword(s):  
Iron Overload ◽  
Iron Age ◽  
Iron Metabolism ◽  
Iron Absorption ◽  
Hereditary Hemochromatosis ◽  
Therapeutic Approaches ◽  
Hepcidin Expression ◽  
Beneficial Effects ◽  
Excess Iron ◽  
Major Factors

Abstract Excess iron deposition in vital organs is the main cause of morbidity and mortality in patients affected by β-thalassemia and hereditary hemochromatosis. In both disorders, inappropriately low levels of the liver hormone hepcidin are responsible for the increased iron absorption, leading to toxic iron accumulation in many organs. Several studies have shown that targeting iron absorption could be beneficial in reducing or preventing iron overload in these 2 disorders, with promising preclinical data. New approaches target Tmprss6, the main suppressor of hepcidin expression, or use minihepcidins, small peptide hepcidin agonists. Additional strategies in β-thalassemia are showing beneficial effects in ameliorating ineffective erythropoiesis and anemia. Due to the suppressive nature of the erythropoiesis on hepcidin expression, these approaches are also showing beneficial effects on iron metabolism. The goal of this review is to discuss the major factors controlling iron metabolism and erythropoiesis and to discuss potential novel therapeutic approaches to reduce or prevent iron overload in these 2 disorders and ameliorate anemia in β-thalassemia.

Dietary iron absorption during early postnatal life

BioMetals ◽  
2019 ◽  
Vol 32 (3) ◽  
pp. 385-393 ◽  
Author(s):  
Sheridan L. Helman ◽  
Gregory J. Anderson ◽  
David M. Frazer
Keyword(s):  
Iron Absorption ◽  
Postnatal Life ◽  
Dietary Iron ◽  
Early Postnatal Life

scholarly journals Hepcidin: A Critical Regulator of Iron Metabolism during Hypoxia

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Korry J. Hintze ◽  
James P. McClung
Keyword(s):  
Iron Metabolism ◽  
Iron Homeostasis ◽  
Molecular Mechanisms ◽  
Iron Absorption ◽  
Iron Acquisition ◽  
Iron Status ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Response Element ◽  
Hypoxia Response ◽  
Hepcidin Expression

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.

Effect of altered iron metabolism on markers of haem biosynthesis and intestinal iron absorption in mice

2004 ◽  
Vol 84 (3) ◽  
pp. 177-182 ◽  
Author(s):  
A. H. Laftah ◽  
K. B. Raja ◽  
G. O. Latunde-Dada ◽  
T. Vergi ◽  
A. T. Mckie ◽  
...  
Keyword(s):  
Iron Metabolism ◽  
Iron Absorption ◽  
Intestinal Iron Absorption ◽  
Haem Biosynthesis

Physiologic systemic iron metabolism in mice deficient for duodenal Hfe

Blood ◽  
2007 ◽  
Vol 109 (10) ◽  
pp. 4511-4517 ◽  
Author(s):  
Maja Vujic Spasic ◽  
Judit Kiss ◽  
Thomas Herrmann ◽  
Regina Kessler ◽  
Jens Stolte ◽  
...  
Keyword(s):  
Iron Metabolism ◽  
Iron Homeostasis ◽  
Iron Absorption ◽  
Binding Capacity ◽  
Hereditary Hemochromatosis ◽  
Direct Interaction ◽  
Hfe Gene ◽  
Hepatic Iron ◽  
Primary Role ◽  
Genes Encoding

Abstract Mutations in the Hfe gene result in hereditary hemochromatosis (HH), a disorder characterized by increased duodenal iron absorption and tissue iron overload. Identification of a direct interaction between Hfe and transferrin receptor 1 in duodenal cells led to the hypothesis that the lack of functional Hfe in the duodenum affects TfR1-mediated serosal uptake of iron and misprogramming of the iron absorptive cells. Contrasting this view, Hfe deficiency causes inappropriately low expression of the hepatic iron hormone hepcidin, which causes increased duodenal iron absorption. We specifically ablated Hfe expression in mouse enterocytes using Cre/LoxP technology. Mice with efficient deletion of Hfe in crypt- and villi-enterocytes maintain physiologic iron metabolism with wild-type unsaturated iron binding capacity, hepatic iron levels, and hepcidin mRNA expression. Furthermore, the expression of genes encoding the major intestinal iron transporters is unchanged in duodenal Hfe-deficient mice. Our data demonstrate that intestinal Hfe is dispensable for the physiologic control of systemic iron homeostasis under steady state conditions. These findings exclude a primary role for duodenal Hfe in the pathogenesis of HH and support the model according to which Hfe is required for appropriate expression of the “iron hormone” hepcidin which then controls intestinal iron absorption.

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