Intestinal Iron Transfer after Ileojejunal Transposition

Digestion ◽  
1991 ◽  
Vol 50 (3-4) ◽  
pp. 182-193 ◽  
Author(s):  
K. Schümann ◽  
B. Elsenhans ◽  
W. Forth ◽  
P. Schroeder
Keyword(s):  
Iron Transfer ◽  
Ileojejunal Transposition

Effect of iron deficiency on placental transfer of iron and expression of iron transport proteins in vivo and in vitro

2001 ◽  
Vol 356 (3) ◽  
pp. 883-889 ◽  
Author(s):  
Lorraine GAMBLING ◽  
Ruth DANZEISEN ◽  
Susan GAIR ◽  
Richard G. LEA ◽  
Zehane CHARANIA ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Transferrin Receptor ◽  
Iron Transport ◽  
Receptor Expression ◽  
Mrna Levels ◽  
Iron Transfer ◽  
Metal Transporter ◽  
Protein Levels ◽  
Copper Oxidase ◽  
Maternal Iron

Maternal iron deficiency during pregnancy induces anaemia in the developing fetus; however, the severity tends to be less than in the mother. The mechanism underlying this resistance has not been determined. We have measured placental expression of proteins involved in iron transfer in pregnant rats given diets with decreasing levels of iron and examined the effect of iron deficiency on iron transfer across BeWo cell layers, a model for placental iron transfer. Transferrin receptor expression was increased at both mRNA and protein levels. Similarly, expression of the iron-responsive element (IRE)-regulated form of the divalent metal transporter 1 (DMT1) was also increased. In contrast, the non-IRE regulated isoform showed no change in mRNA levels. Protein levels of DMT1 increased significantly. Iron efflux is thought to be mediated by the metal transporter protein, IREG1/ferroportin1/MTP1, and oxidation of Fe(II) to Fe(III) prior to incorporation into fetal transferrin is carried out by the placental copper oxidase. Expression of IREG1 was not altered by iron deficiency, whereas copper oxidase activity was increased. In BeWo cells made iron deficient by treatment with desferrioxamine (‘deferioxamine’), iron accumulation from iron-transferrin increased, in parallel with increased expression of the transferrin receptor. At the same time, iron efflux also increased, showing a higher flux of iron from the apical to the basolateral side. The data show that expression of placental proteins of iron transport are up-regulated in maternal iron deficiency, resulting in an increased efficiency of iron flux and a consequent minimization of the severity of fetal anaemia.

scholarly journals Absence of iron transfer from uteroferrin to transferrin.

1986 ◽  
Vol 261 (32) ◽  
pp. 14936-14938
Author(s):  
K Doi ◽  
B C Antanaitis ◽  
P Aisen
Keyword(s):  
Iron Transfer

Hot gun repairs of molten cast iron transfer ladles

Metallurgist ◽  
1969 ◽  
Vol 13 (3) ◽  
pp. 162-163
Author(s):  
A. M. Semenov ◽  
P. I. Andronov ◽  
N. M. Korolev
Keyword(s):  
Cast Iron ◽  
Iron Transfer ◽  
Molten Cast Iron

Increasing the life of mixer-type molten iron transfer ladles

Refractories ◽  
1989 ◽  
Vol 30 (11-12) ◽  
pp. 706-709
Author(s):  
B. A. Kustov ◽  
Yu. A. Marakulin ◽  
S. A. Morozov ◽  
N. A. Pupkov ◽  
Yu. V. Vyazovskii
Keyword(s):  
Molten Iron ◽  
Iron Transfer

Transfer of radioactive iron via the placenta and accessory fetal membranes in the rabbit

1959 ◽  
Vol 197 (1) ◽  
pp. 87-92 ◽  
Author(s):  
J. Davies ◽  
E. B. Brown ◽  
D. Stewart ◽  
C. W. Terry ◽  
J. Sisson
Keyword(s):  
Sharp Increase ◽  
Iron Transport ◽  
Fetal Liver ◽  
Uterine Cavity ◽  
Yolk Sac ◽  
Fetal Membranes ◽  
Steady Increase ◽  
Iron Transfer ◽  
Uterine Mucosa ◽  
Alternative Sites

The distribution of radioactivity in the fetus and placental structures was studied at different stages of gestation in the rabbit following the intravenous injection of radioactive iron as Fe59 sulphate. The following general results were obtained: a) A steady increase in the uptake of radioiron by the fetus and fetal placenta took place with advancing gestation. The rate of uptake showed a sharp increase at about the 20th day. b) The rate of iron transport across the placenta increased during gestation, especially in the last third of pregnancy. c) Radioiron was concentrated in the yolk sac in the early stages and in the fetal liver in the later stages of gestation. No change in the pattern of accumulation of radioiron by the fetus took place when the vessels of the yolk sac were ligated before injection. These results suggest that the yolk sac has no role in iron transport and that early in gestation it may carry on some of the functions of the fetal liver with respect to iron. d) Alternative sites of transport for iron were investigated by the injection of radioiron into the uterine cavity. The results indicate that if iron gains access to the uterine cavity, e.g. via the uterine mucosa or via the chorion and periplacental decidua, it is rapidly absorbed by the yolk sac and enters the fetus. However, such a pathway for iron transfer to the fetus does not seem to be important physiologically.

scholarly journals Hepcidin and iron regulation, 10 years later

Blood ◽  
2011 ◽  
Vol 117 (17) ◽  
pp. 4425-4433 ◽  
Author(s):  
Tomas Ganz
Keyword(s):  
Iron Overload ◽  
Host Defense ◽  
Iron Regulation ◽  
Iron Availability ◽  
Iron Transfer ◽  
Hemoglobin Synthesis ◽  
Metabolic Functions ◽  
Iron Supply ◽  
Infection And Inflammation ◽  
Senescent Erythrocytes

Abstract Under evolutionary pressure to counter the toxicity of iron and to maintain adequate iron supply for hemoglobin synthesis and essential metabolic functions, humans and other vertebrates have effective mechanisms to conserve iron and to regulate its concentration, storage, and distribution in tissues. The iron-regulatory hormone hepcidin, first described 10 years ago, and its receptor and iron channel ferroportin control the dietary absorption, storage, and tissue distribution of iron. Hepcidin causes ferroportin internalization and degradation, thereby decreasing iron transfer into blood plasma from the duodenum, from macrophages involved in recycling senescent erythrocytes, and from iron-storing hepatocytes. Hepcidin is feedback regulated by iron concentrations in plasma and the liver and by erythropoietic demand for iron. Genetic malfunctions affecting the hepcidin-ferroportin axis are a main cause of iron overload disorders but can also cause iron-restricted anemias. Modulation of hepcidin and ferroportin expression during infection and inflammation couples iron metabolism to host defense and decreases iron availability to invading pathogens. This response also restricts the iron supply to erythropoietic precursors and may cause or contribute to the anemia associated with infections and inflammatory disorders.

scholarly journals Maternal iron status influences iron transfer to the fetus during the third trimester of pregnancy

2003 ◽  
Vol 77 (4) ◽  
pp. 924-930 ◽  
Author(s):  
Kimberly O O'Brien ◽  
Nelly Zavaleta ◽  
Steven A Abrams ◽  
Laura E Caulfield
Keyword(s):  
Iron Status ◽  
Third Trimester ◽  
Iron Transfer ◽  
The Third ◽  
Maternal Iron

Intestinal Iron Absorption: Cellular Mechanism and Regulation

Physiology ◽  
1997 ◽  
Vol 12 (4) ◽  
pp. 184-189
Author(s):  
ES Debnam ◽  
SKS Srai
Keyword(s):  
Recent Work ◽  
Brush Border ◽  
Iron Homeostasis ◽  
Iron Absorption ◽  
Cellular Mechanism ◽  
Iron Transfer ◽  
Intestinal Iron Absorption ◽  
Body Iron ◽  
Cellular Processes

Enterocyte iron transfer is crucial for body iron homeostasis, but the cellular processes involved are poorly understood. Recent work suggests the response to increased iron demand involves upregulation of transport at the brush border together with decreased translation of ferritin mRNA, thereby facilitation iron transfer to the blood.

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