Increased intestinal iron absorption in rats with normal hepatic iron stores. Kinetic aspects of the adaptative response to parenteral iron repletion in dietary iron deficiency

Schümann, Klaus; Elsenhans, Bernd; Ehtechami, C.; Förth, W.

doi:10.1016/0304-4165(90)90133-h

Cited by 20 publications

(12 citation statements)

References 22 publications

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“…The timecourse of this response is known from previous studies. A single intravenous dose of 100 mmol Fe´kg body weight 21 is enough to replete liver iron stores in iron-deficient rats within 12 h and to reduce intestinal iron absorption to normal values, though this adaptation takes 48 h [1]. This time-course correlates with the differentiation of duodenal enterocytes, since the migration of [ 3 H]thymidine-labelled enterocytes from the crypts to the villus tips takes 54±59 h [31].…”

Section: Discussionmentioning

confidence: 99%

“…1). The iron supply in the crypts, in turn, is likely to be geared to the body's state of iron repletion [1,42], and IRP may be the intracellular iron sensor, which controls the expression of iron transport proteins in the brush border.…”

Section: Discussionmentioning

confidence: 99%

“…2). This parameter as well as constant transport rates for water and 59 Fe (data not shown here, [1,7,35]) were used to control the viability of the segments.…”

Section: Intestinal Irp Activity At the Crypt±villus Junctions And VImentioning

confidence: 99%

“…The duodenal absorption capacity seems to be geared to the organism's state of iron repletion via changes in mucosal iron supply from the blood side [1]. How intestinal cells sense and adjust iron transport remains, however, largely unknown.…”

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confidence: 99%

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Iron regulatory protein as an endogenous sensor of iron in rat intestinal mucosa

Schümann

Moret²,

Künzle

et al. 1999

European Journal of Biochemistry

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Duodenal enterocytes adjust intestinal iron absorption to the body's state of iron repletion. Here we tested how iron supply from the blood modulates the RNA-binding activity of iron regulatory proteins (IRP-1 and IRP-2) in immature duodenal rat enterocytes, and whether the modulation is compatible with the hypothesis that IRPs, in turn, may regulate the expression of iron transport proteins in maturating enterocytes during migration to the villus tips. Tissue uptake of parenterally applied 59 Fe along the duodenal crypt±villus axis was compared to local IRP-1 and IRP-2 activity and to duodenal 59 Fe transport capacity 12 h, 48 h, and 72 h after intravenous iron administration to iron-deficient rats. IRP-1 and IRP-2 activity was significantly increased in iron-deficiency. 59Fe administrated from the blood side was almost exclusively taken up by crypt enterocytes. Accordingly, the activity of IRP-1 decreased at this site 12 h after parenteral iron administration, but remained high at the villus tips. After 48 h the bulk of 59 Fe containing enterocytes had migrated to the villus tips. Correspondingly, IRP-1 activity was decreased at duodenal villus tips after 48 h. IRP-2 activity also tended to decrease, though the change was statistically not significant. IRP-2 activity remained significantly higher at duodenal villus tips than in crypts, even after 72 h. Intestinal iron absorption capacity decreased with the same delay as IRP-1 activity after intravenous iron administration. In the ileum 59 Fe uptake from the blood and IRP activity showed no significant difference between crypt and villus region. Luminal administration of iron decreased duodenal IRP-1 and IRP-2 activity at tips and crypts within 2 h. Thus, recently absorbed iron becomes available to cytosolic IRP during its passage through the enterocyte. Our results are compatible with a role of IRPs in gearing the expression of intestinal iron transporters in the duodenal brushborder to the body's state of iron repletion.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…2). This parameter as well as constant transport rates for water and 59 Fe (data not shown here, [1,7,35]) were used to control the viability of the segments.…”

Section: Intestinal Irp Activity At the Crypt±villus Junctions And VImentioning

confidence: 99%

mentioning

confidence: 99%

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Iron regulatory protein as an endogenous sensor of iron in rat intestinal mucosa

Schümann

Moret²,

Künzle

et al. 1999

European Journal of Biochemistry

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“…Several investigators reported that one week's feeding of the low iron diet is enough to develop iron deficiency in rats (37,38). Topham and co-workers reported that only 24h of feeding of the low-iron diet result in a 2-fold increase in iron uptake (39).…”

Section: Discussionmentioning

confidence: 99%

Characteristics of Iron Binding to Solubilized Brush Border Membrane of the Rat Intestine.

Ikeda-Moore

Orimo

Hisayasu

et al. 1995

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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Die Rolle des Eisens als Mangelelement

Schümann

1989

Z Ernährungswiss

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Iron is an essential trace element. In its heme-form as well as in its non heme-form it is a part of enzymes and hemoproteins. For a safe and adequate dietary intake 10-18 mg of iron are recommended daily. Frequently, this quantity is not available: approximately 20% of the world population is iron-deficient. In this state the enteral transfer capacity for toxic metals, e.g., Cd and Pb, is increased and the adaptation to physical strain as well as the immunological responses are depressed. Alterations of body iron-stores are almost exclusively balanced by adequate adaptation of the enteral iron-transfer capacity. The mechanism of this adaptation process can neither be satisfactorily explained by the "mucosal block hypothesis", nor by the "mucosal transferrin hypothesis". When the time-course of iron storage and its relation to intestinal iron transfer was investigated after i.v. iron administration to iron-deficient rats, the results indicated that the process of adaptation is located in the intestinal mucosa. Intestinal iron loading is decreased in iron deficiency, whereas the iron transfer into the organism is increased. Further investigation is necessary to find out by which mechanism the iron manages to bypass existing mucosal storage capacity in this situation. The geographical distribution of iron deficiency is influenced by a variety of local factors. Still, the paramount causes of iron-deficiency are unbalanced iron losses and the lack of bioavailable iron in the diet. The bioavailability of non heme iron is influenced by the composition of the diet. The effect of promotors of iron absorption, such as meat, amino acids, polycarbonic acids and ascorbate is opposed by the influence of inhibitors, such as bran, soya products, vegetables and egg-dishes. Iron losses are mainly due to blood losses. Thus, the wide distribution of hookworm diseases in tropical areas contributes significantly to the endemic iron-deficiency in these regions. A more physiological loss of iron is caused by menstruation and pregnancy. In small infants the iron-demand of the organism is increased by rapid growth, which in turn increases the intestinal iron transfer. An increased iron-demand can be balanced by an iron-supplemented diet or by pharmaceutical iron compounds. Acute intoxications can be caused by an overdose of such preparations. The pathophysiology and symptoms of acute iron intoxication are summarized. Their frequency has markedly decreased since "childproof" packaging has been introduced for iron-preparations. To meet the increased iron demand of young children, commercial infant formulas are frequently fortified with iron, preferentially with heme-iron.(ABSTRACT TRUNCATED AT 400 WORDS)

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Increased intestinal iron absorption in rats with normal hepatic iron stores. Kinetic aspects of the adaptative response to parenteral iron repletion in dietary iron deficiency

Cited by 20 publications

References 22 publications

Iron regulatory protein as an endogenous sensor of iron in rat intestinal mucosa

Iron regulatory protein as an endogenous sensor of iron in rat intestinal mucosa

Characteristics of Iron Binding to Solubilized Brush Border Membrane of the Rat Intestine.

Die Rolle des Eisens als Mangelelement

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