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PubMed2006

Body iron and individual iron prophylaxis in pregnancy--should the iron dose be adjusted according to serum ferritin?

This study aims to evaluate iron prophylaxis in pregnant women from the individual aspect, i.e. according to serum ferritin levels at the beginning of pregnancy, and to assess which dose of iron would be adequate to prevent iron deficiency (ID) and iron deficiency anaemia (IDA) during pregnancy and postpartum. A randomised, double-blind study comprising 301 healthy Danish pregnant women allocated into four groups taking ferrous iron (as fumarate) in doses of 20 mg (n=74), 40 mg (n=76), 60 mg (n=77) and 80 mg (n=75) from 18 weeks gestation (inclusion) to 8 weeks postpartum. Iron status markers [serum ferritin, serum soluble transferrin receptor (sTfR), haemoglobin] were recorded at 18, 32 and 39 weeks gestation and 8 weeks postpartum. Body iron was calculated using the serum sTfR/serum ferritin ratio. ID was defined by serum ferritin <12 microg/l in pregnancy and <15 microg/l postpartum; IDA as serum ferritin <12 microg/l and haemoglobin <5th percentile in iron-replete pregnant women. Women in the iron supplement groups were stratified according to serum ferritin levels at inclusion; 50.7% had ferritin 70 microg/l. At 32 weeks, women with ferritin 30 microg/l had an ID frequency of: 20-mg group 20.0%, 40 mg 13.9%, 60 mg 5.7%, 80 mg 5.1% (p<0.001). Women with ferritin >70 microg/l had no ID. Postpartum, ID was found in 4.7% in 20-mg group, 2.9% in group 40 mg and 0% in group 60 and 80 mg. IDA: At 32 weeks, women with ferritin 30 microg/l displayed IDA. Body iron at 18 weeks was 10.4 mg/kg, similar in the four iron groups. Later in pregnancy body iron declined significantly, being lower the 20 mg group, and similar in the 40, 60 and 80-mg groups. Postpartum body iron rose to inclusion levels being 9.3 mg/kg in the 20-mg group and 10.5 mg/kg in the 40-, 60- and 80-mg groups. This study gives an estimate of iron dosage in individual iron prophylaxis adjusted to serum ferritin levels in early pregnancy. In the prevention of ID, we suggest 80-100 mg ferrous iron/day to women having ferritin 70 microg/l have no need for iron supplement.

Adult↗
PubMed2000

Serum ferritin iron in iron overload and liver damage: correlation to body iron stores and diagnostic relevance.

The iron content of serum ferritin has been determined in groups of patients with normal or increased iron stores by using a technique of ferritin immunoprecipitation followed by iron quantitation with atomic absorption spectroscopy. The results were correlated to individual liver iron concentrations, measured non-invasively by superconducting quantum interference device (SQUID) biomagnetometry. A close correlation between serum concentrations of ferritin protein and ferritin iron was found (r = 0.92) in all groups of patients. However, the correlation between ferritin iron concentration and individual liver iron concentration was poor in patients with hemochromatosis (r = 0.63) and patients with beta-thalassemia major (r = 0.57). The degree of ferritin iron saturation was about 5% in iron-loaded patients, which contrasts with results in two recent studies but confirms older observations. In patients with liver cell damage, the ferritin iron saturation in serum was significantly higher than that found in groups with iron overload disease, probably indicating the release of intracellular iron-rich ferritin into the blood. The monitoring of patients undergoing bone marrow transplantation indicated that the release of iron-rich and iron-poor ferritin occurred during phases of hepatocellular damage and inflammation, respectively. We find the benefits of serum ferritin iron measurement to be marginal in patients with iron overload disease.

Adult↗
PubMed2002

Initial uptake and absorption of nonheme iron and absorption of heme iron in humans are unaffected by the addition of calcium as cheese to a meal with high iron bioavailability.

BACKGROUND: Quantitative data on the mucosal uptake and serosal transfer of nonheme-iron absorption in humans and the effects of calcium on these components are limited. OBJECTIVE: Our objective was to measure the initial mucosal uptake and the subsequent serosal transfer of nonheme iron and to determine the effects of adding calcium to a meal on both heme- and nonheme-iron retention. DESIGN: Whole-gut lavage and whole-body scintillation counting methods were applied to determine the 8-h uptake of nonheme iron and the 2-wk retention (absorption) of heme and nonheme iron in healthy adults (n = 17) after the consumption of meals of radiolabeled food. RESULTS: The initial uptake and absorption of nonheme iron were 11% and 7%, respectively, and the absorption of heme iron was 15%. Two-thirds of the nonheme iron taken up by the mucosa within 8 h was retained by the body after 2 wk (serosal transfer index: 0.63). Serum ferritin correlated inversely with the initial uptake and absorption of nonheme iron, but not with the nonheme serosal transfer index or the absorption of heme iron. Adding calcium (127 mg in cheese) to the meal did not affect absorption. CONCLUSIONS: On the basis of its association with serum ferritin, the initial mucosal uptake was the primary control point for nonheme-iron absorption. An apparent reduction in heme-iron absorption associated with the lavage procedure suggested that uptake of heme iron may take longer and proceed further through the intestine than that of nonheme iron. The absorption of both forms of iron was unaffected by the addition of cheese to this meal with high iron bioavailability.

Administration, Oral↗
PubMed1985

Iron absorption in normal and iron-deficient beagle dogs: mucosal iron kinetics.

Absorption of dietary iron requires uptake of iron by the brush border of the intestinal epithelial cells, intracellular transport, and transfer to the systemic circulation. In iron-deficiency anemia, iron absorption is greatly increased, but the individual steps responsible for this increase have not been identified. We have developed a method to evaluate the rate constants for each of these steps, and we report here our results in beagle dogs a) under normal conditions and b) after phlebotomy to produce iron-deficiency anemia. Simultaneous administration of oral 59Fe3+-citrate and intravenous 55Fe-transferrin was used to investigate the kinetics of mucosal iron transport. Plasma levels of both isotopes and the whole-body excretion pattern of 59Fe were monitored sequentially, and the fractional mucosal transport rates were estimated by nonlinear least-squares fit of a physiologically based mathematical model to these data. Under normal conditions the fractional rate of mucosal iron uptake from the intestinal lumen was rate limiting, being less than 1% of the fractional rate of either iron incorporation into the mucosal storage pool or transfer of iron from the mucosa to the plasma. After induction of iron-deficiency anemia, the fractional mucosal iron uptake rate increased sixfold (P less than 0.005), while the rate of incorporation into the mucosal storage pool decreased ninefold (P less than 0.02); in contrast, the fractional rate of iron transfer to the plasma did not change. These results indicate that the enhanced iron absorption in iron-deficiency anemia is attributable to an increase in mucosal iron available for transfer to the plasma, leading in turn to a net increase in iron absorption, despite a normal fractional transfer rate.

Anemia, Hypochromic↗
PubMed2001

Iron-fortified and unfortified cow's milk: effects on iron intakes and iron status in young children.

UNLABELLED: Iron intakes and iron status were evaluated in 36 young Swedish children given either iron-fortified or unfortified cow's milk. All children had good iron status and had received breast milk or iron-fortified formulae during infancy. Twenty 1-y-old children were randomized to a diet with iron-fortified milk (7.0 or 14.9 mg Fe l(-1) and 16 to a diet with unfortified milk. The iron intakes in the unfortified group at 15 and 18 mo (mean +/- SD 5.19 +/- 2.29 and 5.84 +/- 1.62 mg d(-1)) were low in relation to Nordic Nutrition Recommendations, while the intakes in the iron-fortified group (10.20 +/- 2.60 and 10.87 +/- 2.79mg d(-1)) were normal in relation to recommendations. The gain (increase) from receiving fortified diet during the study period was at most [upper limit for 95% confidence interval (CI)] 2.6 g l(-1) in blood haemoglobin, 1.9 fl in mean corpuscular volume, 2.7 micromol in serum iron and 4.5% in transferrin iron saturation, and the gain (decrease) was at most (lower limit for 95% CI) 0.29g l(-1) in serum transferrin and 0.9mg l(-1) in serum transferrin receptor (TfR). None of these differences was statistically significant. There was an almost significantly higher increase in serum ferritin (1.4 times higher relation of values at the end compared with the beginning, p = 0.06) and a significantly higher (1.2; p = 0.047) decrease in TfR/ log10 ferritin ratio in the fortified group. CONCLUSION: One-year-old children starting out with good iron status given either iron-fortified or unfortified cow's milk from 12 to 18 mo maintain sufficient iron status during this period. However, children fed unfortified cow's milk have an iron intake which is low in relation to recommendations and the quantitative development of their reserve iron in iron stores seems to be weaker than that of the fortified group. The consequences of this require further study.

Animals↗
PubMed2003

Duodenal mucosal reductase in wild-type and Hfe knockout mice on iron adequate, iron deficient, and iron rich feeding.

BACKGROUND: Genetic haemochromatosis is a common hereditary iron loading disorder in humans. The disease is associated with loss of function mutations in the HFE gene. This is thought to change iron stores via increased iron absorption. AIMS: In this study we investigated how adaptation of mucosal reductase activity is engaged in this process and how the changes compare with adaptation seen when an iron deficient diet is fed. METHODS: Duodenal mucosal surface reductase was measured with nitroblue tetrazolium in age matched groups of male Hfe knockout mice (Hfe) and wild- type mice fed a purified diet containing normal (iron adequate), high (iron rich), or low (iron deficient) iron concentrations. RESULTS: Reductase activity increased when mice were fed an iron deficient diet and decreased when they were fed an iron rich diet. Total villus activity, as measured by the average area under the activity curve along the crypt-villus axis, was increased 2.8-2.9-fold by iron deficiency in both genotypes. Approximately half of this difference was attributable to the significantly increased length of the villi in mice on an iron deficient diet (p<0.05). Hfe knockout did not affect villus length but increased mucosal reductase activity near the villus tips. Similar increases (1.3-1.6-fold) were seen on all diets but the increase was significant for iron deficient and iron loaded diets only (p<0.05). CONCLUSION: Hfe gene product and dietary iron downregulate villus reductase activity in mice.

Animals↗
PubMed1992

Salivary iron status in children with iron deficiency and iron overload.

Forty anaemic (iron deficiency anaemia-27, thalassemia major-8, and aplastic anaemia-5) and 10 non-anaemic children (serving as controls) aged from 8 months to 10 years were selected for the study. The salivary iron was significantly higher in iron deficient and iron overload conditions compared to controls. The mean salivary:serum iron ratio was same in control and iron overload cases, while it was twice as high in iron deficient anaemic children. The correlation between salivary iron and serum iron was significant (r = 0.7392, P less than 0.001) in these cases. The iron deficient anaemic children with hypoalbuminaemia had significantly reduced serum and salivary protein (P less than 0.001), but iron concentrations in serum and saliva remained unaltered. The salivary protein level had significant correlations with serum albumin and serum protein (P less than 0.001). Thus, the iron in saliva is maintained at a higher level and more so in iron deficiency anaemia; it correlates well with serum iron (r = 0.6853, P less than 0.001) in iron deficient anaemic children also and is not affected by co-existing hypoproteinaemic situation.

Albumins↗
PubMed2003

The effect of iron therapy on the growth of iron-replete and iron-deplete children.

This prospective, double-blind, placebo-controlled trial was designed to study the effect of iron therapy on the growth of iron-replete and iron-deficient children, and to study the change in iron status in iron-deficient children with iron therapy. One hundred and fifty children (aged 6-24 months) were included in the study. After an informed written consent, 100 healthy children, who were iron replete (group I) according to preset criteria, were randomly allocated to receive iron supplements 2 ng/kg/day (group IA) or placebo (group IB). Fifty iron-deficient children (group II) were administered iron syrup 6 mg/kg/day. Growth parameters (weight, length and head-circumference) and hematological parameters were studied for 4 months. Iron therapy, as compared with placebo, produced a significant improvement of mean monthly weight gain (p < 0.001) and linear growth (p < 0.001) in the iron-deficient children. However, it significantly decreased the weight gain (p < 0.001) and linear growth (p < 0.001) of iron-replete children. Caution should therefore be exercised while supplementing iron to children with apparently normal growth and when the iron status of the child is not known.

Anemia, Iron-Deficiency↗
PubMed2005

In vitro evaluation of iron solubility and dialyzability of various iron fortificants and of iron-fortified milk products targeted for infants and toddlers.

The objectives of the present study were: to compare the solubility and dialyzability of various iron fortificants (iron pyrophosphate, ferrous bis-glycinate, ferrous gluconate, ferrous lactate, ferrous sulfate) added, in the presence of ascorbic acid, to pasteurized milk samples produced under laboratory conditions; and to compare the solubility and dialyzability of iron in commercial pasteurized, UHT and condensed milk products available in the Greek market fortified with various vitamins and minerals including iron and targeted towards infants (6-12 months old) and toddlers. Iron solubility and dialyzability were determined using a simulated gastrointestinal digestive system. Ferrous dialyzable iron (molecular weight lower than 8000) was used as an index for prediction of iron bioavailability. Ferrous dialyzable iron in pasteurized milk samples fortified with iron pyrophosphate, ferrous lactate and ferrous bis-glycinate was higher (P < 0.05) than that in milk samples fortified with ferrous sulfate and ferrous gluconate. In commercial liquid pasteurized or UHT milk products, formation of ferrous dialyzable iron in products fortified with ferrous lactate was not different (P > 0.05) from those fortified with ferrous sulfate. Ferrous dialyzable iron in four condensed commercial milk products was higher (P < 0.05) than the corresponding values of the liquid UHT milk samples fortified with the same fortificant (ferrous sulfate). Ferrous dialyzable iron was higher (P < 0.05) in products targeted for infants compared with those targeted for toddlers. In conclusion, the type of iron source, milk processing and the overall product composition affect formation of ferrous dialyzable iron and may determine the success and effectiveness of iron fortification of milk.

Animals↗
PubMed1989

Biochemistry of nonheme iron in man. I. Iron proteins and cellular iron metabolism.

Total plasma iron turnover in man is about 36 mg/day. Transferrin is the iron transport protein of plasma, which can bind 2 atoms of iron per protein molecule, and which interacts with various cell types to provide them with the iron required for their metabolic and proliferative processes. All tissues contain transferrin receptors on their plasma membrane surfaces, which interact preferentially with diferric transferrin. In erythroid cells as well as certain laboratory cell lines, the removal of iron from transferrin apparently proceeds via the receptor-mediated endocytosis process. Transferrin and its receptor are recycled to the cell surface, whereas the iron remains in the cell. The mode of iron uptake in the hepatocyte, the main iron storage tissue, is less certain. The release of iron by hepatocytes, as well as by the reticuloendothelial cells, apparently proceeds nonspecifically. All tissues contain the iron storage protein ferritin, which stores iron in the ferric state, though iron must be in the ferrous state to enter and exit the ferritin molecule. Cellular cytosol also contains a small-molecular-weight ferrous iron pool, which may interact with protoporphyrin to form heme, and which apparently is the form of iron exported by hepatocytes and macrophages. In plasma, the ferrous iron is converted into the ferric form via the action of ceruloplasmin.

Animals↗
PubMed1981

Serum iron and total iron-binding capacity compared with serum ferritin in assessment of iron deficiency.

Ferritin values for 250 selected sera were compared with values for iron, total iron-binding capacity (TIBC), and transferrin saturation, to assess the potential of the ferritin assay for the detection of latent iron deficiency. The specimens were grouped (50 in each group) according to their values for iron and TIBC. In Group 1 (low iron, high TIBC) the saturation and ferritin values both indicated iron deficiency in all but one. In the 100 specimens of Groups 2 (normal iron, high TIBC) and 4 (normal iron, high normal TIBC), the saturation values revealed 16 iron-deficient cases, the ferritin test 55. For Groups 3 (low iron, normal TIBC) and 5 (low iron, low TIBC), the ferritin test revealed fewer cases of iron deficiency than did the saturation values (37 cases vs 51 cases, in the 100 specimens). Evidently the ferritin test detects iron deficiency in many cases for whom the serum iron and TIBC tests are not positively indicative. The correlation of serum ferritin with iron, TIBC, and transferrin saturation in the five groups was good only in the case of specimens for which the TIBC was normal; if it was abnormal the correlation was very poor.

Anemia, Hypochromic↗
PubMed2004

The effect of alcohol consumption on the prevalence of iron overload, iron deficiency, and iron deficiency anemia.

BACKGROUND & AIMS: Our aim was to investigate the relationship between alcohol consumption and iron overload, iron deficiency, or iron deficiency anemia in the U.S. population. METHODS: Adult participants of the Third National Health and Nutrition Examination Survey who did not consume alcohol (n = 8839) were compared with participants who consumed < or =1 (n = 4976), >1 to < or =2 (n = 1153), or >2 (n = 915) alcoholic drinks/day during the preceding 12 months. We examined the following markers of iron overload: elevated serum transferrin-iron saturation (TS) level (>45%, >50%, and >60%), elevated serum ferritin level (>300, >400, >500, and >600 ng/mL), and combinations of both elevated serum TS and ferritin levels. Iron deficiency was defined as the presence of at least 2 of the following: serum ferritin level <12 ng/mL, serum TS level <15%, and erythrocyte protoporphyrin level >1.24 micromol/L. Iron deficiency anemia was defined as the presence of both iron deficiency and anemia. RESULTS: Compared with nondrinkers, the prevalence of all markers of iron overload was significantly elevated among those who consumed >2 alcoholic drinks/day after adjusting for potential confounders. Consumption of any amount of alcohol was associated with a 40% reduction in the risk of iron deficiency anemia. CONCLUSIONS: Consumption of up to 2 alcoholic drinks/day seems to be associated with reduced risk of iron deficiency and iron deficiency anemia without a concomitant increase in the risk of iron overload. Consumption of >2 alcoholic drinks/day is associated with a significant elevation in the risk of iron overload.

Adolescent↗
PubMed2005

Expression of iron-acquisition-related genes in iron-deficient rice is co-ordinately induced by partially conserved iron-deficiency-responsive elements.

Rice plants (Oryza sativa L.) utilize the iron chelators known as mugineic acid family phytosiderophores (MAs) to acquire iron from the rhizosphere. Synthesis of MAs and uptake of MA-chelated iron are strongly induced under conditions of iron deficiency. Microarray analysis was used to characterize the expression profile of rice in response to iron deficiency at the genomic level. mRNA extracted from iron-deficient or iron-sufficient rice roots or leaves was hybridized to a rice array containing 8987 cDNA clones. An induction ratio of greater than 2.0 in roots was observed for 57 genes, many of which are involved in iron-uptake mechanisms, including every identified or predicted step in the methionine cycle and the biosynthesis of MAs from methionine. Northern analysis confirmed that the expression of genes encoding every step in the methionine cycle is thoroughly induced by iron deficiency in roots, and almost thoroughly induced in leaves. A promoter search revealed that the iron-deficiency-induced genes related to iron uptake possessed sequences homologous to the iron-deficiency-responsive cis-acting elements IDE1 and IDE2 in their promoter regions, at a higher rate than that showing no induction under Fe deficiency. These results suggest that rice genes involved in iron acquisition are co-ordinately regulated by conserved mechanisms in response to iron deficiency, in which IDE-mediated regulation plays a significant role.

Blotting, Northern↗
PubMed2005

Comparative assessment of the bioavailability, efficacy and safety of a modified-release (MR) carbonyl iron tablet and oral conventional iron preparation in adult Indian patients with nutritional iron deficiency anaemia.

The objective of the study is to evaluate the bioavailability, efficacy and safety of a new modified-release (MR) formulation of carbonyl iron (45 mg) relative to a commercially available conventional formulation of ferrous fumarate (300 mg) in adult Indian patients with clinical and laboratory diagnosis of nutritional iron deficiency anaemia. This prospective, comparative, randomised, double-blind study was carried out among 60 patients received a single daily dose of either MR carbonyl iron or ferrous fumarate for 12 weeks. The effect of therapy on haematological parameters and iron status and estimation of bioavailability were the main efficacy outcomes. There was a significant (p<0.05) increase in mean haemoglobin levels, reticulocyte counts, haematocrit and mean corpuscular volume in MR carbonyl iron group compared to ferrous fumarate group. There was also an increase in mean serum iron and ferritin levels and a corresponding decrease in total iron binding capacity in MR carbonyl iron group compared to ferrous fumarate group at the end of 12 weeks therapy. The estimated overall bioavailability of MR carbonyl iron was about 147% that of ferrous fumarate. Both the formulations were equally well-tolerated and adverse events were mainly gastrointestinal in nature. The prevalence of adverse events was slightly more in the ferrous fumarate group. It can be concluded that the MR formulation of carbonyl iron was more efficacious than ferrous fumarate in correcting haematologic abnormalities and improving iron status in patients with nutritional iron deficiency anaemia. In conditions where efficacy is an important consideration, the higher bioavailability of MR carbonyl iron may make it the treatment of choice for nutritional iron deficiency anaemia.

Administration, Oral↗
PubMed2007

Effects of wheat flour fortified with different iron fortificants on iron status and anemia prevalence in iron deficient anemic students in Northern China.

OBJECTIVES: To compare the effects of wheat flours fortified with NaFeEDTA, FeSO4 and elemental iron (electrolytic iron), in improving iron status in anemic students. METHODS: Four hundreds anemic students (11 to 18 years old) were divided into four groups and given wheat flour fortified with different iron fortificants at different concentrations: control group (no added iron); NaFeEDTA group (20 mg Fe/kg); FeSO4 group (30 mg Fe/kg); and elemental iron group (60 mg Fe/kg). The trial lasted for 6 months and the following parameters were examined every 2 months: whole blood hemoglobin, free erythrocyte protoporphyrin, serum ferritin, serum iron, total iron binding capacity and transferrin receptor. RESULTS: The flour consumption in the 4 groups was 300-400 g/person/day, accounted for 70% of total cereal consumption in the diets. There were no significant differences in flour consumption among the 4 groups. Blood hemoglobin level increased in all the 3 intervened groups, but the increment in the NaFeEDTA group was significantly higher and earlier than the other 2 groups; and only 1% of the subjected remained anemic at the end of the trial in the NaFeEDTA group, while 40% and 60% of the subjects in the FeSO4 and electrolytic iron group remained anemic, respectively. The order of improvements in free erythrocyte protoporphyrin, serum ferritin and transferring receptor levels were: NaFeEDTA > FeSO4 > electrolytic iron. No significant changes were found in the control group on all the tested parameters during the trial. CONCLUSIONS: The results indicated that even NaFeEDTA was added at a lower level, it has better effects than FeSO4 and elemental iron on controlling iron deficiency anemia and improving iron status in anemic children; while elemental iron was the least effective.

Adolescent↗
PubMed1991

Lactoferrin inhibits or promotes Legionella pneumophila intracellular multiplication in nonactivated and interferon gamma-activated human monocytes depending upon its degree of iron saturation. Iron-lactoferrin and nonphysiologic iron chelates reverse monocyte activation against Legionella pneumophila.

We have been exploring the role of iron in the pathogenesis of the intracellular bacterial pathogen Legionella pneumophila. In previous studies, we have demonstrated that L. pneumophila intracellular multiplication in human monocytes is iron dependent and that IFN gamma-activated monocytes inhibit L. pneumophila intracellular multiplication by limiting the availability of iron. In this study, we have investigated the effect on L. pneumophila intracellular multiplication of lactoferrin, an iron-binding protein which is internalized via specific receptors on monocytes, and of nonphysiologic iron chelates which enter monocytes by a receptor-independent route. Apolactoferrin completely inhibited L. pneumophila multiplication in nonactivated monocytes, and enhanced the capacity of IFN gamma-activated monocytes to inhibit L. pneumophila intracellular multiplication. In contrast, iron-saturated lactoferrin had no effect on the already rapid rate of L. pneumophila multiplication in nonactivated monocytes. Moreover, it reversed the capacity of activated monocytes to inhibit L. pneumophila intracellular multiplication, demonstrating that L. pneumophila can utilize iron from the lactoferrin-lactoferrin receptor pathway. The capacity of iron-lactoferrin to reverse monocyte activation was dependent upon its percent iron saturation and not just its total iron content. Similarly, the nonphysiologic iron chelates ferric nitrilotriacetate and ferric ammonium citrate completely reverse and ferric pyrophosphate partially reversed the capacity of IFN gamma-activated monocytes to inhibit L. pneumophila intracellular multiplication, demonstrating that L. pneumophila can utilize iron derived from nonphysiologic iron chelates internalized by monocytes independently of the transferrin and lactoferrin endocytic pathways. This study suggests that at sites of inflammation, lactoferrin may inhibit or promote L. pneumophila intracellular multiplication in mononuclear phagocytes depending upon its degree of iron saturation. In addition, this study suggests a potential role for PMN in host defense against L. pneumophila--providing apolactoferrin to infected monocytes--and it supports the concept that PMN and monocytes may cooperate in host defense against intracellular parasites and other pathogens.

Apoproteins↗
PubMed1990

Response of various indices of iron status to acute iron depletion produced in menstruating women by low iron intake and phlebotomy.

We investigated response sensitivities of indices of iron status to controlled iron depletion and repletion in 11 premenopausal women. The women were depleted of storage iron (as reflected by serum ferritin) through a combination of a low-iron diet and phlebotomy. They then consumed a diet containing 13.7 mg of iron per 2000 kcal, supplemented with either ascorbic acid or placebo (for 5 1/2 weeks) and a daily 50-mg iron supplement (for the subsequent 17 days). The relative sensitivities of different indices for detecting iron depletion were as follows: ferritin greater than % transferrin saturation greater than plasma iron greater than hemoglobin greater than hematocrit greater than zinc protoporphyrin (ZnPP) and erythrocyte protoporphyrin (EP). Ascorbic acid treatment during repletion, before iron supplementation, significantly (P less than 0.05) affected changes in hemoglobin, ZnPP, ZnPP/heme, and EP/heme. Changes in heme synthesis evidently do not occur until iron stores are depleted and, conversely, during iron repletion hematopoiesis must be satisfied before iron stores, as reflected by ferritin, increase. Thus, the use of only one index of iron status is of limited value for detecting iron depletion.

Adult↗
PubMed1995

[Transferrin receptor and iron deposition pattern in the hepatic lobules of the iron-deficient and iron-overloaded rats].

Wistar rats were made iron deficient by a low iron regimen. Iron overload was produced by repeated intraperitoneal injections of ferric nitrilotriacetate (Fe(3+)-NTA) for one to four months. Hepatic tissues from these iron deficient, overloaded and control rats were examined for transferrin receptor (TfR), transferrin (Tf) and iron after immunohistochemical staining. TfR and Tf were mainly distributed in the peripheral part of the lobule (zone 1) in the normal, iron deficient and iron-overloaded rats. The staining intensity decreased from zone 1 to zone 3. The staining intensity of TfR was strongest in iron-deficiency rat hepatic cells, weakest in iron-overloaded rat hepatic cells when compared with controls. The difference of Tf staining between the three groups of rats was similar to that of TfR. In the iron-overloaded rats, the staining intensity of iron was stronger in zone 1 than in zone 2 and 3, similar to the distribution pattern of TfR and Tf. These findings suggest that (1) iron uptake in hepatic cells in vivo is regulated and mediated by TfR and Tf, (2) the expression pattern of TfR and Tf in zone 1 to zone 3 liver cells may result in the progressive decrease of iron deposition in the hepatic lobules of the iron overloaded rats.

Anemia, Iron-Deficiency↗