scholarly journals Molecular liaisons between erythropoiesis and iron metabolism

Blood ◽  
2014 ◽  
Vol 124 (4) ◽  
pp. 479-482 ◽  
Author(s):  
Leon Kautz ◽  
Elizabeta Nemeth
Keyword(s):  
Blood Plasma ◽  
Iron Metabolism ◽  
Iron Absorption ◽  
Iron Distribution ◽  
Plasma Iron ◽  
Iron Supply ◽  
Tissue Iron ◽  
Made In ◽  
In Blood Plasma ◽  
Iron Concentrations

Abstract Although most circulating iron in blood plasma is destined for erythropoiesis, the mechanisms by which erythropoietic demand modulates the iron supply (“erythroid regulators”) remain largely unknown. Iron absorption, plasma iron concentrations, and tissue iron distribution are tightly controlled by the liver-produced hormone hepcidin. During the last decade, much progress has been made in elucidating hepcidin regulation by iron and inflammation. This review discusses the less understood mechanisms and mediators of hepcidin suppression in physiologically and pathologically stimulated erythropoiesis.

scholarly journals Regulation of iron absorption and storage iron turnover

Blood ◽  
1980 ◽  
Vol 56 (1) ◽  
pp. 30-37
Author(s):  
A Rosenmund ◽  
S Gerber ◽  
H Huebers ◽  
C Finch
Keyword(s):  
Iron Absorption ◽  
Iron Concentration ◽  
Iron Release ◽  
Plasma Iron ◽  
Iron Supply ◽  
Tissue Iron ◽  
Iron Deficient ◽  
Humoral Mechanism ◽  
And Storage ◽  
Male Rate

The regulation of iron supply to plasma was studied in male rate. Repeated exchange transfusions were first carried out with plasma from iron-deficient or iron-loaded animals. There was no recognizable effect on the amount of iron entering the plasma as evidenced by plasma iron concentration or iron absorption by recipient animals. In other studies, iron compounds having different tissue distribution were injected. Subsequent iron release was greater from reticuloendothelial cells than from other iron-loaded tissues. When requirements for transferrin iron were increased by exchange transfusion with high reticulocyte blood, within minutes there was a doubling of the rate of tissue iron donation. It was concluded from these studies that (1) iron turnover in the plasma is primarily determined by the number of tissue receptors for iron, particularly those of the erythron, (2) that the amount of iron supplied by each donor tissue is dependent on the output of other donor tissues, and (3) that a humoral mechanism regulating iron exchange is unlikely in view of the speed of response and magnitude of changes in plasma iron turnover. It is proposed that there is some direct mechanism that determines the movement of iron from donor tissues to unsaturated transferrin binding sites.

scholarly journals Crosstalk between Iron Metabolism and Erythropoiesis

2010 ◽  
Vol 2010 ◽  
pp. 1-12 ◽  
Author(s):  
Huihui Li ◽  
Yelena Z. Ginzburg
Keyword(s):  
Iron Deficiency ◽  
Iron Metabolism ◽  
Iron Absorption ◽  
Hereditary Hemochromatosis ◽  
Beta Thalassemia ◽  
Key Factors ◽  
Hemoglobin Synthesis ◽  
Iron Supply ◽  
Models Of Disease ◽  
Made In

Iron metabolism and erythropoiesis are inextricably linked. The majority of iron extracted from circulation daily is used for hemoglobin synthesis. In the last 15 years, major advances have been made in understanding the pathways regulating iron metabolism. Hepcidin is a key regulator of iron absorption and recycling and is itself regulated by erythropoiesis. While several viable candidates have been proposed, elucidating the “erythroid regulator” of hepcidin continues to generate significant experimental activity in the field. Although the mechanism responsible for sensing iron demand for erythropoiesis is still incompletely understood, evaluating diseases in which disordered erythropoiesis and/or iron metabolism are showcased has resulted in a more robust appreciation of potential candidates coordinated erythroid iron demand with regulators of iron supply. We present data drawn from four different conditions—iron deficiency, congenital hypotransferrinemia, beta-thalassemia, and hereditary hemochromatosis—both in human and non-human models of disease, together suggesting that erythroid iron demand exerts a stronger influence on circulating iron supply than systemic iron stores. Greater understanding of the interplay between the key factors involved in the regulation of iron metabolism and erythropoiesis will help develop more effective therapies for disorders of iron overload, iron deficiency, and hemoglobin synthesis.

scholarly journals Regulation of iron absorption and storage iron turnover

Blood ◽  
1980 ◽  
Vol 56 (1) ◽  
pp. 30-37 ◽  
Author(s):  
A Rosenmund ◽  
S Gerber ◽  
H Huebers ◽  
C Finch
Keyword(s):  
Iron Absorption ◽  
Iron Concentration ◽  
Iron Release ◽  
Plasma Iron ◽  
Iron Supply ◽  
Tissue Iron ◽  
Iron Deficient ◽  
Humoral Mechanism ◽  
And Storage ◽  
Male Rate

Abstract The regulation of iron supply to plasma was studied in male rate. Repeated exchange transfusions were first carried out with plasma from iron-deficient or iron-loaded animals. There was no recognizable effect on the amount of iron entering the plasma as evidenced by plasma iron concentration or iron absorption by recipient animals. In other studies, iron compounds having different tissue distribution were injected. Subsequent iron release was greater from reticuloendothelial cells than from other iron-loaded tissues. When requirements for transferrin iron were increased by exchange transfusion with high reticulocyte blood, within minutes there was a doubling of the rate of tissue iron donation. It was concluded from these studies that (1) iron turnover in the plasma is primarily determined by the number of tissue receptors for iron, particularly those of the erythron, (2) that the amount of iron supplied by each donor tissue is dependent on the output of other donor tissues, and (3) that a humoral mechanism regulating iron exchange is unlikely in view of the speed of response and magnitude of changes in plasma iron turnover. It is proposed that there is some direct mechanism that determines the movement of iron from donor tissues to unsaturated transferrin binding sites.

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 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 Ineffective erythropoiesis in β-thalassemia is characterized by increased iron absorption mediated by down-regulation of hepcidin and up-regulation of ferroportin

Blood ◽  
2007 ◽  
Vol 109 (11) ◽  
pp. 5027-5035 ◽  
Author(s):  
Sara Gardenghi ◽  
Maria F. Marongiu ◽  
Pedro Ramos ◽  
Ella Guy ◽  
Laura Breda ◽  
...  
Keyword(s):  
Iron Overload ◽  
Iron Content ◽  
Iron Absorption ◽  
Regulatory Gene ◽  
Regulatory Genes ◽  
Ineffective Erythropoiesis ◽  
Transfusion Therapy ◽  
Iron Distribution ◽  
Tissue Iron

Abstract Progressive iron overload is the most salient and ultimately fatal complication of β-thalassemia. However, little is known about the relationship among ineffective erythropoiesis (IE), the role of iron-regulatory genes, and tissue iron distribution in β-thalassemia. We analyzed tissue iron content and iron-regulatory gene expression in the liver, duodenum, spleen, bone marrow, kidney, and heart of mice up to 1 year old that exhibit levels of iron overload and anemia consistent with both β-thalassemia intermedia (th3/+) and major (th3/th3). Here we show, for the first time, that tissue and cellular iron distribution are abnormal and different in th3/+ and th3/th3 mice, and that transfusion therapy can rescue mice affected by β-thalassemia major and modify both the absorption and distribution of iron. Our study reveals that the degree of IE dictates tissue iron distribution and that IE and iron content regulate hepcidin (Hamp1) and other iron-regulatory genes such as Hfe and Cebpa. In young th3/+ and th3/th3 mice, low Hamp1 levels are responsible for increased iron absorption. However, in 1-year-old th3/+ animals, Hamp1 levels rise and it is rather the increase of ferroportin (Fpn1) that sustains iron accumulation, thus revealing a fundamental role of this iron transporter in the iron overload of β-thalassemia.

Iron Metabolism in the Pregnant Rabbit

1958 ◽  
Vol 193 (3) ◽  
pp. 615-622 ◽  
Author(s):  
Thomas H. Bothwell ◽  
Walther F. Pribilla ◽  
Winston Mebust ◽  
Clement A. Finch
Keyword(s):  
Iron Metabolism ◽  
Concentration Gradient ◽  
Iron Transport ◽  
Maternal Plasma ◽  
Active Process ◽  
Plasma Iron ◽  
Placental Transport ◽  
Pregnant Rabbit ◽  
Maternal Metabolism ◽  
Made In

Studies on iron metabolism were made in pregnant rabbits. The amount of iron transported from the maternal plasma to fetus increased progressively with age and weight of the fetus. By the end of the pregnancy 90% of the plasma iron turnover was directed to the fetus. The majority of fetal iron is deposited as nonhemoglobin iron. Placental iron transport occurs against a concentration gradient. The uptake of iron by the placenta is an active process independent of the fetus, and retrograde transfer of iron from the fetus to mother does not occur. Studies of altered maternal metabolism indicate that placental transport reflects both fetal demands and state of iron metabolism in the mother.

scholarly journals Is iron deficiency involved in the pathogenesis of chronic inflammatory skin disorders?

2019 ◽  
Vol 73 ◽  
pp. 359-363
Author(s):  
Małgorzata Ponikowska ◽  
Jacek C. Szepietowski
Keyword(s):  
Iron Deficiency ◽  
Iron Metabolism ◽  
Reticuloendothelial System ◽  
The Body ◽  
Iron Stores ◽  
Iron Supply ◽  
Tissue Iron ◽  
Bowel Disorders ◽  
Dermatological Disorders ◽  
Dermatologic Disease

Iron is an essential microelement in the human body due to its role in hematopoiesis, involvement in energetic processes, synthesis and decomposition of lipids, proteins and nuclear acids. Iron deficiency (ID) is common in healthy populations and also frequently coincides with natural course of chronic diseases. The former is typically present when the overall iron body storages are exhausted (absolute ID), most often due to insufficient iron supply, malabsorption or increased blood loss and coincides with anemia. The latter is a result of defected iron metabolism and reflects a condition, when despite adequate iron stores in the body, iron itself is trapped in the reticuloendothelial system, becoming unavailable for the metabolic processes. It typically occurs in the presence proinflammtory activation in chronic conditions such as chronic kidney disease, inflammatory bowel disorders, malignancies and heart failure. To date there are very few publications concerning the potential role of ID in chronic dermatological disorders. We have recently found that patients with psoriasis demonstrate pattern of ID which can be characterized by negative tissue iron balance with depleted iron stores in the body. Interestingly, presence of ID was not related to the severity of psoriasis, but rather determined by patients low body mass index. We are currently investigating the hypothesis that derangements in iron metabolism resulting in ID can be also present in hidradenitis suppurativa – the other chronic dermatologic disease associated with inflammatory and autoimmune activation.

scholarly journals Dynamics of changes in iron concentration and total iron binding capacity in blood plasma of goat kids during their first month of life (Short Communication)

2009 ◽  
Vol 52 (4) ◽  
pp. 419-424
Author(s):  
W. F. Skrzypczak ◽  
M. Ożgo ◽  
A. Lepczyński ◽  
A. Łata
Keyword(s):  
Blood Plasma ◽  
Binding Capacity ◽  
Iron Concentration ◽  
Total Iron ◽  
Postnatal Life ◽  
Iron Binding ◽  
Total Iron Binding Capacity ◽  
Plasma Iron ◽  
Iron Binding Capacity ◽  
In Blood Plasma

Abstract. The experiment was carried out on 14 kids of Polish Improved White breed during the first 30 days of life. The aim of this study was to show changes in the concentration of blood plasma iron and total iron binding capacity (TIBC) during the neonatal period. The statistically confirmed differences (P≥0.01) in blood serum iron concentration was show in the kids between 5th (20.57 μmol/l) and 14th (9.97 μmol/l) day of life, and between 3rd and 4th week with the peak in 23rd day (27.50 μmol/l). We have also shown statisticly confirmed increase in TIBC (P≥0.01) between 1st and 4th day of life (+20.13 μmol/l), and between 14th and 23rd day of life (+15.59 μmol/l). Statistically confirmed decrease of TIBC was observed between 6th (52.30 μmol/l) and 14th (31.78 μmol/l) day of life. Conclusion: The studies have revealed dynamic changes in the concentration and total binding capacity of blood plasma iron concentration during the first month of postnatal life. The pattern of such changes does not depend on the gender or litter size. It was observed a significant decrease in the concentration of this trace element in blood plasma toward the end of the second week, which may indicate a relative iron deficiency, particularly in twin-born kids.

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