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

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.

Blood ◽  
1980 ◽  
Vol 56 (1) ◽  
pp. 30-37 ◽  
Author(s):  
A Rosenmund ◽  
S Gerber ◽  
H Huebers ◽  
C Finch

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.


Blood ◽  
1986 ◽  
Vol 67 (3) ◽  
pp. 623-628 ◽  
Author(s):  
J Edwards ◽  
H Huebers ◽  
C Kunzler ◽  
C Finch

Iron metabolism in the Belgrade rat was examined in the intact animal and in the reticulocyte suspensions. The plasma iron turnover was increased. However, when allowance was made for the effect of the elevated plasma iron concentration, erythroid marrow capacity for iron uptake was at basal levels. Numbers of erythroid cells in marrow and spleen measured by the radioiron dilution technique were increased. Thus iron uptake was not proportionate to the erythroid hyperplasia in the b/b rat, despite a more than adequate plasma iron supply. This relative deficiency in iron uptake was reflected in a severe microcytosis and elevated red cell protoporphyrin. Reticulocyte incubation studies demonstrated an unimpaired uptake of the transferrin- iron-receptor complex but a marked reduction in iron accumulation. The diferric transferrin molecule, when it did give up iron within the cell, released both of its iron atoms so that only apotransferrin was returned to the media. In contrast to the nearly complete release of iron within the normal reticulocyte, the major portion of iron taken up by the Belgrade reticulocyte was returned to the plasma. The release mechanism that can be impaired in iron-deficient reticulocytes by EDTA or cadmium was shown to be affected by lower concentrations of these substances in the Belgrade reticulocyte. It is concluded that the Belgrade rat has an abnormality of iron release within the absorptive vacuole that is responsible for a state of intracellular iron deficiency, involving the erythron and other body tissues.


Blood ◽  
1986 ◽  
Vol 67 (3) ◽  
pp. 623-628 ◽  
Author(s):  
J Edwards ◽  
H Huebers ◽  
C Kunzler ◽  
C Finch

Abstract Iron metabolism in the Belgrade rat was examined in the intact animal and in the reticulocyte suspensions. The plasma iron turnover was increased. However, when allowance was made for the effect of the elevated plasma iron concentration, erythroid marrow capacity for iron uptake was at basal levels. Numbers of erythroid cells in marrow and spleen measured by the radioiron dilution technique were increased. Thus iron uptake was not proportionate to the erythroid hyperplasia in the b/b rat, despite a more than adequate plasma iron supply. This relative deficiency in iron uptake was reflected in a severe microcytosis and elevated red cell protoporphyrin. Reticulocyte incubation studies demonstrated an unimpaired uptake of the transferrin- iron-receptor complex but a marked reduction in iron accumulation. The diferric transferrin molecule, when it did give up iron within the cell, released both of its iron atoms so that only apotransferrin was returned to the media. In contrast to the nearly complete release of iron within the normal reticulocyte, the major portion of iron taken up by the Belgrade reticulocyte was returned to the plasma. The release mechanism that can be impaired in iron-deficient reticulocytes by EDTA or cadmium was shown to be affected by lower concentrations of these substances in the Belgrade reticulocyte. It is concluded that the Belgrade rat has an abnormality of iron release within the absorptive vacuole that is responsible for a state of intracellular iron deficiency, involving the erythron and other body tissues.


Blood ◽  
2014 ◽  
Vol 124 (4) ◽  
pp. 479-482 ◽  
Author(s):  
Leon Kautz ◽  
Elizabeta Nemeth

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.


Blood ◽  
1978 ◽  
Vol 52 (1) ◽  
pp. 187-195 ◽  
Author(s):  
AC Chou ◽  
GO Jr Broun ◽  
CD Fitch

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.


Blood ◽  
1981 ◽  
Vol 57 (2) ◽  
pp. 239-242 ◽  
Author(s):  
W Bauer ◽  
S Stray ◽  
H Huebers ◽  
C Finch

Abstract Plasma iron turnover has been evaluated in the growing rat. Consistent data were obtained with the intravenous injection of radioiron in the form of ferrous sulfate or ferric citrate. Plasma iron turnover changed as a function of plasma iron concentration. Only part of this effect in the rat was due to the different rates of clearance of mono-and differic transferrin, the latter having a higher iron delivery rate in vivo. An additional effect was shown to relate to the rate of red cell production. With decreased production, the effect of plasma iron on plasma iron turnover was reduced, whereas with increased erythropoiesis there was an additional increment in plasma iron turnover for any increase in plasma iron. Since this effect was observed when increased iron demands were due to an increase in erythroid precursors in the marrow but not in the circulating blood, it is attributed to limitations in iron flow to the marrow. This suggests that erythroid marrow activity and the adequacy of iron supply when studied by ferrokinetic techniques can best be defined by the response curve relating plasma iron concentration to plasma iron turnover.


1964 ◽  
Vol 207 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Georg W. Strohmeyer ◽  
Stephen A. Miller ◽  
Robert W. Scarlata ◽  
Edward W. Moore ◽  
Mortimer S. Greenberg ◽  
...  

Rats exposed to an atmosphere of 10% oxygen increase their absorption of a test dose of iron after 6 8 hr. Release of tissue storage iron begins within 2 hr of the start of hypoxia and continues for at least 8 hr. An oral iron load does not prevent the release of tissue iron in response to hypoxia. Iron-loaded rats also release iron from storage depots and increase their minimal absorption in response to hypoxia. Iron-deficient rats apparently have a diminished tissue release and also increase absorption above their elevated base-line levels. Xanthine loading had no effect on the release of tissue iron or changes in absorption with hypoxia, and there was no evidence that changes in xanthine oxidase activity in the liver or bowel were directly associated with tissue release or absorption of iron.


Blood ◽  
1983 ◽  
Vol 61 (4) ◽  
pp. 799-802 ◽  
Author(s):  
T Uchida ◽  
T Akitsuki ◽  
H Kimura ◽  
T Tanaka ◽  
S Matsuda ◽  
...  

A circadian rhythm was demonstrated in 10 males and 10 females with respective mean decreases in plasma iron concentration at 18 hr of 62% and 47% of morning values. Ferrokinetic studies performed on 5 normal males and 5 normal females showed a more rapid disappearance rate and lower plasma iron turnover in the evening. Parallel studies were done on 6 normal males in the morning and 4 normal males in the evening of the release of reticuloendothelial iron at 8 and 18 hr after intravenous injection of 59Fe chondroitin ferrous sulfate. The 6-hr release in the morning was 54.1% and in the evening 25.9%. Composite data from morning and evening showed a correlation between plasma iron level and plasma iron turnover (r = 0.76, p less than 0.001). A similar correlation existed between the plasma iron level and the percent of radioiron released from the reticuloendothelial system (r = 0.67, 0.02 less than p less than 0.05). These data are consistent with a fluctuating iron release from the reticuloendothelial cell in normal subjects, which would account for the diurnal variation in plasma iron.


Blood ◽  
1981 ◽  
Vol 57 (2) ◽  
pp. 239-242
Author(s):  
W Bauer ◽  
S Stray ◽  
H Huebers ◽  
C Finch

Plasma iron turnover has been evaluated in the growing rat. Consistent data were obtained with the intravenous injection of radioiron in the form of ferrous sulfate or ferric citrate. Plasma iron turnover changed as a function of plasma iron concentration. Only part of this effect in the rat was due to the different rates of clearance of mono-and differic transferrin, the latter having a higher iron delivery rate in vivo. An additional effect was shown to relate to the rate of red cell production. With decreased production, the effect of plasma iron on plasma iron turnover was reduced, whereas with increased erythropoiesis there was an additional increment in plasma iron turnover for any increase in plasma iron. Since this effect was observed when increased iron demands were due to an increase in erythroid precursors in the marrow but not in the circulating blood, it is attributed to limitations in iron flow to the marrow. This suggests that erythroid marrow activity and the adequacy of iron supply when studied by ferrokinetic techniques can best be defined by the response curve relating plasma iron concentration to plasma iron turnover.


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