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At least 19 recordsLinked to original sources
PubMed2001

Body iron stores and iron restoration rate in Japanese patients with chronic hepatitis C as measured during therapeutic iron removal revealed neither increased body iron stores nor effects of C282Y and H63D mutations on iron indices.

Information on the level of iron stores in chronic hepatitis C is clinically important because its reduction is technically simple and therapeutically effective. This study was performed to measure the levels of iron stores from the total amounts of hemoglobin removed during iron reduction therapy. The C282Y and H63D mutations of HFE gene were analyzed in 94 patients. All of the patients were negative for C282Y mutation. One patient was homozygous, and 4 patients were heterozygous for H63D mutation. The body iron stores and iron restoration rate were measured in 59 patients in serial courses of iron reduction therapy. Mean values of body iron stores in the two groups with and without H63D mutation were 890 and 606 mg, while those of iron restoration rate were 1.85 and 1.52 mg/day, respectively. None of the indices of iron metabolism were different from the reference values measured similarly in healthy subjects, suggesting that the iron deposition in chronic hepatitis C is limited to the liver, probably due to changes in the iron distribution in tissues.

Female↗
PubMed1980

[Studies on iron metabolism and iron deficiency anemia in pregnant women--theoretical discussion on the relation between serum iron level and iron dose to be administrate, and clinical result after iron therapy (author's transl)].

Animal and clinical studies were performed in order to establish a criterion for diagnosis of iron-deficiency anemia and a standard dose of the intravenous iron treatment, based on properties of serum transferrin (Tr) in ironmetabolism during gestation. And the following results were obtained. 1) 59Fe-labelled large molecular colloid iron-solution (CSA-Fe) was injected in pregnant rats: the iron transferring to the fetuses originated from the mothers' serum iron isolated from CSA-Fe. 2) There was no difference of iron supplying abilities of Tr across to maternal and fetal tissues of rat, in anemia in the latter stage of gestation (A) and in non-pregnant iron-deficiency anemia (B), although there was significant difference in nature of Tr between rat and woman. 3) Tr of rat in A and in B: There was no difference in 59Fe-uptake into the rat reticulocytes from Tr between the two statuses. 4) In the clinical study, iron utilization rate was correlated with serum iron saturation rate both in A and B. 5) CSA-Fe was clinically given for A and B according to the original formulas, and utility of the formulas were confirmed.

Anemia, Hypochromic↗
PubMed2000

Iron stores and haemoglobin iron deficits in menstruating women. Calculations based on variations in iron requirements and bioavailability of dietary iron.

BACKGROUND: Iron stores and haemoglobin iron deficits in menstruating women can be calculated from body iron losses and absorption of dietary iron using recently developed methods. OBJECTIVE: To examine iron balance (iron status) expressed as body iron stores or haemoglobin iron deficits in menstruating women from amounts of iron lost (iron requirements) and amounts of dietary iron absorbed. Calculations are made both of stationary states and of the rate of changes in iron stores (iron status) when any of the two main factors determining iron balance are changed. DESIGN: The study is based on (1) previous and new equations describing relationships between iron absorption, iron requirements (losses), iron stores and/or haemoglobin deficits and (2) published data on iron requirements and their variation in menstruating adult women. RESULTS: Both iron stores and haemoglobin iron deficits are strongly related to iron requirements and absorption of dietary iron and follow the same equations during states of iron repletion and iron deficiency. When, for example, increasing or decreasing the bioavailability of the dietary iron, about 90% of the change in iron stores will occur within 1 y. CONCLUSIONS: There are strong relationships between iron requirements, bioavailability of dietary iron and amounts of stored iron. The observations that a reduction in iron stores and a calculated decrease of haemoglobin iron had the same increasing effect on iron absorption suggest that the control of iron absorption is mediated from a common cell, that may register both size of iron stores and hemoglobin iron deficit, eg the hepatocyte. European Journal of Clinical Nutrition (2000) 54, 650-657.

Absorption↗
PubMed2000

Iron excretion in iron-overloaded rats following the change from an iron-loaded to an iron-deficient diet.

BACKGROUND: Iron stores in the body are thought to be regulated by a mechanism associated with the rate of iron absorption from the diet, with no significant role played by iron excretion. We report the existence of an iron excretory process that results in the loss of significant amounts of liver iron. METHODS AND RESULTS: Rats were fed 3% carbonyl iron for 9 weeks, which resulted in a 20-fold increase in liver non-haem iron. When the rats on this iron-loaded diet were switched to a low iron diet for 2 and 7 days, liver non-haem iron levels fell 30% and 45%, respectively. A similar fall in transferrin-bound plasma iron was also seen. As the liver iron had not redistributed to other body compartments, it was concluded that the iron had been excreted and that the excreted iron represented a loss of 22% and 28% in total body non-haem iron over 2 and 7 days, respectively. Ligation of the common bile duct in iron loaded rats that had been switched to the iron-deficient diet was accompanied by a similar loss of liver iron and also hepatocellular damage. In addition, measurement of enterocyte iron levels showed that only approximately 5% of the total iron excreted was found in these cells. CONCLUSION: Neither bile nor enterocytes play a significant role in iron excretion. The similarity in the degree of fall in transferrin-bound iron levels with a change in diet suggests that iron excretion involves the uptake and excretion of transferrin bound-iron, possibly by goblet cells. The observed hypertrophy of the intestinal mucosa associated with carbonyl iron feeding may facilitate hypersecretion of mucous and the excretion of this iron.

Animals↗
PubMed1990

Colorimetry and constant-potential coulometry determinations of transferrin-bound iron, total iron-binding capacity, and total iron in serum containing iron-dextran, with use of sodium dithionite and alumina columns.

After the parenteral administration of iron-dextran (imferon), the increased total iron concentrations in serum can be determined by atomic absorption spectroscopy and by colorimetric methods involving sodium dithionite, which reductively dissociates iron from the dextran complex. We report that constant-potential coulometry detects only about 55-70% of dextran-bound iron before dithionite reduction and variable amounts after reaction with the reducing agent. In addition, we have developed a procedure for determining transferrin-bound iron, total iron-binding capacity (TIBC), total iron, and dextran-bound iron with the Kodak Ektachem colorimetric system. In determining total serum iron, the sample is first mixed with sodium dithionite, which rapidly dissociates all dextran-bound iron, but does not remove iron from either transferrin or hemoglobin. After the mixture is applied to an Ektachem slide, transferrin-bound iron is released at pH 4 and is detected together with the iron previously bound to dextran. TIBC is determined by mixing serum with ferric citrate in moderate excess and filtering through a small alumina (Al2O3) column, which binds excess free iron and iron-dextran; the iron in the column eluate represents the TIBC. Transferrin-bound iron is determined by applying diluted serum without added ferric citrate to an alumina column and measuring the iron in the column eluate. Dextran-bound iron is equivalent to the difference between total and transferrin-bound iron. Using this method, we found that transferrin iron-binding sites are saturated in vitro by excess iron-dextran less efficiently than by ferric citrate.

Aluminum Oxide↗
PubMed2003

Evaluation of myocardial iron by magnetic resonance imaging during iron chelation therapy with deferrioxamine: indication of close relation between myocardial iron content and chelatable iron pool.

Evaluation of myocardial iron during iron chelation therapy is not feasible by repeated endomyocardial biopsies owing to the heterogeneity of iron distribution and the risk of complications. Recently, we described a noninvasive method based on magnetic resonance imaging. Here, the method was used for repeated estimation of the myocardial iron content during iron chelation with deferrioxamine in 14 adult nonthalassemic patients with transfusional iron overload. We investigated the repeatability of the method and the relationship between the myocardial iron estimates and iron status. The repeatability coefficient (2sD) was 2.8 micromol/g in the controls (day-to-day) and 4.0 micromol/g in the patients (within-day). Myocardial iron estimates were elevated in 10 of all 14 patients at first examination, but normalized in 6 patients after 6 to 18 months of treatment. If liver iron declined below 350 micromol/g all but one of the myocardial iron estimates were normal or nearly normal. At start (R2 = 0.69, P =.0014) and still after 6 months of iron chelation (R2 = 0.76, P =.001), the estimates were significantly and more closely related to the urinary iron excretion than to liver iron or serum ferritin levels. In conclusion, our preliminary data, which may only pertain to patients with acquired anemias, suggest the existence of a critical liver iron concentration, above which elevated myocardial iron is present, but its extent seems related to the size of the chelatable iron pool, as reflected by the urinary iron excretion. This further supports the concept of the labile iron pool as the compartment directly involved in transfusional iron toxicity.

Adult↗
PubMed2002

Iron status in Danish men 1984-94: a cohort comparison of changes in iron stores and the prevalence of iron deficiency and iron overload.

BACKGROUND AND OBJECTIVES: From 1954 to 1987, flour in Denmark was fortified with 30 mg carbonyl iron per kg. This mandatory fortification was abolished in 1987. The aim of this study was to compare iron status in Danish men before and after abolition of iron fortification. METHODS: Iron status (serum ferritin, haemoglobin), was assessed in population surveys in Copenhagen County during 1983-84 comprising 1324 Caucasian men (1024 non-blood-donors, 300 blood donors) and in 1993-94 comprising 1288 Caucasian men (1103 non-blood-donors, 185 donors), equally distributed in age cohorts of 40, 50, 60 and 70 yr. RESULTS: In the 1984 survey median serum ferritin values in the four age cohorts in non-blood-donors were 136, 141, 133 and 111 microg/L, and in the 1994 survey 177, 173, 186 and 148 microg L(-1), respectively. The difference was significant in all age groups (P<0.001). There was no significant difference between the two surveys concerning the prevalence of small iron stores (ferritin 16-32 micro g L(-1)), depleted iron stores (ferritin <16 microg L(-1)) or iron-deficiency anaemia (ferritin <13 microg L(-1) and Hb <5th percentile for iron-replete men). However, from 1984 to 1994, the prevalence of iron overload (ferritin >300 microg L(-1)) increased from 11.3% to 18.9% (P<0.0001). During the study period there was an increase in body mass index (P<0.0001), alcohol consumption (P<0.03) and use of non-steroid anti-inflammatory drugs (NSAID) (P<0.0001), and a decrease in the use of vitamin-mineral supplements (P<0.04) and in the prevalence of tobacco smoking (P<0.0001). In contrast, median ferritin in blood donors showed a significant fall from 1984 to 1994 (103 vs. 74 micro g L(-1), P<0.02). CONCLUSION: Abolition of iron fortification reduced the iron content of the Danish diet by an average of 0.24 mg MJ(-1), and the median dietary iron intake in men from 17 to 12 mg d(-1). From 1984 to 1994, body iron stores and the prevalence of iron overload in Danish men increased significantly, despite the abolition of food iron fortification. The reason appears to be changes in dietary habits, with a lower consumption of dairy products and eggs, which inhibit iron absorption, and a higher consumption of alcohol, meat, and poultry, containing haem iron and enhancing iron absorption. The high prevalence of iron overload in men may constitute a health risk.

Adult↗
PubMed2000

Iron status in Danes 1994. II: Prevalence of iron deficiency and iron overload in 1319 Danish women aged 40-70 years. Influence of blood donation, alcohol intake and iron supplementation.

Iron status, i.e. serum ferritin and haemoglobin (Hb) levels, was assessed in a population survey in 1994 (Dan-Monica 10) comprising 1319 Caucasian Danish women in age cohorts of 40, 50, 60 and 70 years. In the entire series, ferritin levels increased significantly from 40 years to 60 years of age. The prevalence of small iron stores (ferritin 16-32 microg/l), depleted iron stores (ferritin < 16 microg/l) and of iron deficiency anaemia (ferritin < 13 microg/l and Hb < 121 g/l) decreased steadily with age. Blood donors (n = 109) had lower ferritin levels than non-donors (P<0.0001). Ferritin levels in donors were inversely correlated with the cumulated number of lifetime phlebotomies (r(s) = -0.25, P<0.01). Ferritin levels in non-donors (n = 1208) were low in 40-year-old women (median 40 microg/l) and increased to a median of 95 microg/l in 60- and 70-year-old women (P<0.0001). In non-donors 40 years of age, the prevalence of small iron stores was 40.4%, the prevalence of depleted iron stores 10.8% and the prevalence of iron deficiency anaemia 2.16%. The prevalence of iron overload (ferritin >300 microg/l) was 1.54%. Ferritin levels in 60- and 70-year-old non-donors were correlated with the body mass index (r(s) =0.11, P=0.01). Ferritin levels in 50- to 60-year-old non-donors were correlated with alcohol intake (r(s)=0.23, P<0.0001). In the entire series, 37.5% of non-donors took supplemental ferrous iron (median 14 mg iron per day). Iron supplements had a significant positive influence on iron status in 40-year-old premenopausal non-donors but no effect in postmenopausal women or in donors. Non-donors (n = 170) treated with acetylsalicylic acid had lower ferritin levels (median 55 microg/l) than non-treated (n = 1038; median 75 microg/l) (P<0.0001). Compared with the Dan-Monica 1 iron status survey in 1984, the prevalence of iron deficiency and iron deficiency anaemia was unchanged, whereas the prevalence of iron overload displayed a slight increase. The 1987 abolition of the mandatory iron fortification of flour apparently had no negative effect on iron status.

Adult↗
PubMed1990

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.

Male Sprague-Dawley rats were fed an iron-deficient diet for 8 days. After this period, iron stores were repleted in three groups of animals by intravenous administration of iron dextran. In a second set of experiments, iron was administered in the same dose as Fe nitrilotriacetic acid complex. 12 h, 24 h and 48 h thereafter, the intestinal iron transfer in vitro and in vivo as well as the non-heme iron and ferritin content were determined in both the liver and the jejunal mucosa. In iron deficiency, intestinal iron transfer is increased to 230% of untreated controls, while non-heme iron and ferritin decreased to 20% and 10% in the liver and to 55% and 25% in the mucosa, respectively. 12 h and 24 h after parenteral administration of 0.1 mmol Fe/kg body weight iron transfer was as high as in iron deficiency, while liver iron stores were not significantly different from the untreated controls. In this situation, the close link between decreases in body iron stores and increases in iron transfer was temporarily dissociated. This can be related to the time lag between the incorporation of parenterally applied iron in the liver and in the jejunal mucosa. The data provide evidence for the hypothesis that the hepatic iron stores have no means of neural or hormonal communication with the small intestine in order to adapt iron transfer to their state of repletion on short notice. Intestinal iron transfer returned to control levels after 48 h.

Adaptation, Physiological↗
PubMed2000

Adaptation in iron absorption: iron supplementation reduces nonheme-iron but not heme-iron absorption from food.

BACKGROUND: Results of cross-sectional studies suggest that in healthy people, iron absorption adapts to meet physiologic needs and stabilize iron stores, but this has not been adequately tested in longitudinal studies. OBJECTIVE: We tested whether heme- and nonheme-iron absorption decrease in response to increased iron intake and whether iron stores reach a steady state. DESIGN: In a randomized, placebo-controlled trial, heme- and nonheme-iron absorption by healthy men and women (n = 57) were measured before and after 12 wk of supplementation with 50 mg Fe/d as ferrous sulfate. Serum and fecal ferritin were measured during supplementation and for 6 mo thereafter. RESULTS: Initially, both heme- and nonheme-iron absorption were inversely associated with serum ferritin concentration. Volunteers who took iron supplements, even those with serum ferritin <21 microg/L (n = 5), adapted to absorb less nonheme iron (3.2% at week 12 compared with 5.0% at week 0, P: < 0.001) but not less heme iron from a beef-based meal. Serum ferritin concentration was slightly but significantly higher after iron supplementation than after placebo (difference = 13 microg/L). This higher ferritin concentration persisted for >/=6 mo after supplementation, except in subjects with low iron stores, whose serum ferritin returned to baseline within 3 mo. Fecal ferritin excretion increased 2.5-fold (P: < 0.05) during supplementation. CONCLUSIONS: Healthy individuals, even those with low iron stores, had reduced nonheme-iron absorption from food in response to iron supplementation. Despite this partial adaptation, iron stores were greater after iron supplementation than after placebo and this difference was sustained, except in individuals with the lowest iron stores.

Adaptation, Physiological↗
PubMed1984

Chronic experimental iron losses in rats not leading to overt iron deficiency: a model for the regulation of the whole-body iron balance in an iron-replete condition.

Intestinal iron absorption studies, which include investigation of iron deficiency, increased erythropoiesis, low iron diet and acute bleeding, have been done, but none have reported the regulation of the balance of an iron-replete individual. We bled rats at regular time intervals, such that the experimentally induced iron losses were compensated by iron from storage and nutritional procurement without the onset of anemia. During these experimental periods the hemoglobin and plasma iron concentrations were determined along with repeated histochemical gradings of the bone marrow iron. We determined the intestinal iron absorption at regular intervals after having established its relation to the intragastric ferrous iron dose. The results obtained show that regular bleedings of 15-20% of the total blood volume every 10 days or twice a week, respectively, are compensated completely by storage and nutritional iron procurement without the onset of anemia. The intestinal iron absorption is increased 4 hours after an acute bleeding and was found high during the period that the animals were bled every 10 days. Significant changes of the plasma iron concentration, mostly within the "normal range" are invariably associated with experimental changes in bleeding regimes. The observed increases of the intestinal absorption of a ferrous iron test dose and decreases of the plasma iron concentrations that precede the depletion of the histochemically graded bone marrow iron are interpreted by a modification of a reported model, in which the process of iron release into the plasma from the reticuloendothelial system and the gut mucosa is linked closely to the actual plasma iron concentration.

Animals↗
PubMed1999

Iron status in Danes updated 1994. I: prevalence of iron deficiency and iron overload in 1332 men aged 40-70 years. Influence Of blood donation, alcohol intake, and iron supplementation.

Iron status, S-ferritin, and hemoglobin (Hb) were assessed in a population survey in 1994 (DAN-MONICA 10) comprising 1332 Caucasian Danish men equally distributed in age cohorts of 40, 50, 60 and 70 years. Blood donors (n=186) had lower S-ferritin, median 76 microg/l, than nondonors, median 169 microg/l (p<0.0001). S-ferritin in donors was inversely correlated with the number of phlebotomies (r(s)=-0.57, p<0.0001). S-ferritin in nondonors (n=1146) was similar in men 40-60 years of age, median 176 microg/l, and subsequently decreased at 70 years of age to a median of 146 microg/l (p=0.01). In the entire series, the prevalence of small iron stores (S-ferritin 16-32 microg/l) was 2.7%, that of depleted iron stores (S-ferritin <16 microg/l) 0.45%, and that of iron deficiency anemia (S-ferritin <13 microg/l and Hb <129 g/l) 0.15%. Among nondonors, the prevalence of iron overload (S-ferritin >300 microg/l) was 20%. S-ferritin in nondonors correlated with body mass index (r(s)=0.19, p=0.0001) and with alcohol intake (r(s)=0.26, p=0.0001). In the entire series, 28% of the subjects took supplemental iron (median 14 mg ferrous iron daily). Iron supplements had no influence on iron status. Nondonors (n=170) treated with acetylsalicylic acid had lower S-ferritin, median 136 microg/l, than nontreated, median 169 microg/l (p<0.001) and those treated with H(2)-receptor antagonists (n=30) had lower S-ferritin, median 142 microg/l, than nontreated, median 171 microg/l (p<0.04). Compared with the DAN-MONICA 1 iron status survey of Danish men in 1984, the prevalences of iron depletion and iron deficiency anemia are unchanged whereas the prevalence of iron overload has increased significantly. In Denmark, iron fortification of flour was abolished in 1987. This apparently had no negative effect on iron status in men.

Adult↗
PubMed2003

Iron supplementation during infancy--effects on expression of iron transporters, iron absorption, and iron utilization in rat pups.

BACKGROUND: Studies conducted in human infants suggest developmental changes in the regulation of iron absorption; however, little is known about the molecular mechanisms regulating iron absorption during infancy. Two intestinal iron transporters, divalent metal transporter 1 (DMT1) and ferroportin 1 (FPN1), were recently identified. OBJECTIVE: The objective was to investigate at a molecular level the regulation of iron absorption during infancy in a rat pup model. We examined the developmental expression of DMT1 and FPN1 and the effects of iron supplementation on their expression and on iron absorption and utilization during infancy. DESIGN: Rat pups were given daily oral doses of 0, 30, or 150 microg Fe from day 2 to day 20 after birth. On days 10 and 20 after birth, (59)Fe absorption, tissue minerals, and intestinal DMT1, FPN1, and ferritin expression were examined. To assess developmental expression, DMT1 and FPN1 were examined in control rats from days 1 to 50 after birth. RESULTS: Intestinal DMT1 and FPN1 were significantly affected by age; expression increased dramatically by day 40. On day 10, no significant effect of iron supplementation on DMT1 and FPN1 gene expression or on iron absorption was observed. By day 20, DMT1 and FPN1 expression and iron absorption had decreased significantly with iron supplementation. CONCLUSIONS: During early infancy, rat pups are unable to down-regulate intestinal iron transporters or iron absorption in response to iron supplementation, whereas down-regulation occurs during late infancy. The current findings provide evidence of the developmental regulation of iron absorption, which emphasizes the need for caution when giving iron supplements to infants at an early age.

Age Factors↗
PubMed2003

Iron status in Danish women, 1984-1994: a cohort comparison of changes in iron stores and the prevalence of iron deficiency and iron overload.

BACKGROUND AND OBJECTIVES: From 1954 to 1986, flour in Denmark was fortified with 30 mg carbonyl iron per kilogram. This mandatory enrichment of cereal products was abolished in 1987. The aim was to evaluate iron status in the Danish female population before and after abolishment of iron fortification. METHODS: Iron status, serum ferritin and haemoglobin, was assessed in population surveys in 1983-1984 comprising 1221 Caucasian women (1089 non-blood-donors, 130 donors) and in 1993-1994 comprising 1261 women (1155 non-blood-donors, 104 donors) equally distributed in age cohorts of 40, 50, 60 and 70 yr. RESULTS: In the 1984 survey, median ferritin values in the four age cohorts in non-blood-donors were 44, 57, 84 and 80 microg/L, and in the 1994 survey 40, 67, 97 and 95 microg/L, respectively. In 1984, premenopausal women had median ferritin of 43 microg/L and in 1994 of 39 microg/L (NS). In 1984, postmenopausal women had median ferritin of 75 microg/L and in 1994 of 93 microg/L (P < 0.0001). The prevalence of depleted iron stores (ferritin < 16 microg/L) was not significantly different in 1984 and 1994 either in premenopausal or in postmenopausal women. The prevalence of small + depleted iron stores (ferritin 300 microg/L) was unchanged in premenopausal women and had increased from 2.4% to 5.5% in postmenopausal women (P = 0.003). During the study period there was an increase in body mass index both in premenopausal and postmenopausal women (P = 0.06 and P = 0.008). Postmenopausal women displayed an increase in alcohol consumption (P < 0.0001) and a decrease in tobacco smoking (P < 0.001). In premenopausal women, there was a marked increase in the use of non-steroid anti-inflammatory drugs (P < 0.0001) in the study period, while this was unchanged in postmenopausal women. In premenopausal blood donors, median ferritin decreased from 1984 to 1994 (36 microg/L vs. 24 microg/L, P < 0.06). In postmenopausal blood donors, ferritin was not significantly different from 1984 to 1994 (50 microg/L vs. 41 microg/L, P = 0.15). CONCLUSION: Abolition of iron fortification reduced the median dietary iron intake in Danish women from 12 to 9 mg/d. Despite the absence of food iron fortification, from 1984 to 1994, body iron stores were unchanged in premenopausal women, whereas iron stores and the prevalence of iron overload in postmenopausal women had increased significantly. The reason appears to be the changes in dietary habits with a lower consumption of dairy products and eggs, which inhibit iron absorption, and a higher consumption of alcohol, meat and poultry, containing heme iron and enhancing iron absorption.

Adult↗
PubMed1995

True absorption and retention of supplemental iron is more efficient when iron is administered every three days rather than daily to iron-normal and iron-deficient rats.

Absorption of daily iron supplements is inefficient. Detailed absorption patterns of FeSO4 supplements simulating World Health Organization-recommended doses were studied in iron-deficient and iron-normal male Sprague-Dawley rats. For 12 d after weaning, the rats were fed a premeal containing < 20 (iron-deficient group) or 400 micrograms Fe (iron-normal group) twice daily followed by iron-free AIN-76 diet for 1 h. Then, both groups (iron-deficient and -normal) were divided in three groups, one continuing without change and two receiving 4000 micrograms of premeal Fe either daily or every 3 d to match intestinal mucosa renewal time. Food intake, growth, hemoglobin concentration and periodic 59Fe-labeled iron absorption and rate of loss were determined. Iron-deficient rats became anemic, and ate and grew less. Iron absorption was stable in normal (34.2%), deficient (89.7%) and normal, intermittently supplemented (9.5%) groups. Absorption decreased logarithmically in daily supplemented rats, whereas in iron-deficient, intermittently supplemented rats absorption decreased slowly and linearly. Rates of iron loss were significantly accelerated in daily supplemented rats. Thirteen-day total iron retention in intermittently supplemented normal and deficient rats was 62 and 86%, respectively, of that of daily supplemented rats. Iron supplementation timed to match mucosal renewal is more efficient.

Absorption↗
PubMed1999

Influence of prenatal iron and zinc supplements on supplemental iron absorption, red blood cell iron incorporation, and iron status in pregnant Peruvian women.

BACKGROUND: It is estimated that 60% of pregnant women worldwide are anemic. OBJECTIVE: We aimed to examine the influence of iron status on iron absorption during pregnancy by measuring supplemental iron absorption, red blood cell iron incorporation, and iron status in pregnant women. DESIGN: Subjects were 45 pregnant Peruvian women (33+/-1 wk gestation), of whom 28 received daily prenatal supplements containing 60 mg Fe and 250 microg folate without (Fe group, n = 14) or with (Fe+Zn group, n = 14) 15 mg Zn, which were were consumed from week 10 to 24 of gestation until delivery. The remaining 17 women (control) received no prenatal supplementation. Iron status indicators and isotopes were measured in maternal blood collected 2 wk postdosing with oral (57Fe) and intravenous (58Fe) stable iron isotopes. RESULTS: Maternal serum ferritin and folate concentrations were significantly influenced by supplementation (P < 0.05). Serum iron was also significantly higher in the Fe than in the Fe+Zn (P < 0.03) or control (P < 0.001) groups. However, the supplemented groups had significantly lower serum zinc concentrations than the control group (8.4+/-2.3 and 10.9+/-1.8 micromol/L, respectively, P < 0.01). Although percentage iron absorption was inversely related to maternal serum ferritin concentrations (P = 0.036), this effect was limited and percentage iron absorption did not differ significantly between groups. CONCLUSIONS: Because absorption of nonheme iron was not substantially greater in pregnant women with depleted iron reserves, prenatal iron supplementation is important for meeting iron requirements during pregnancy.

Administration, Oral↗
PubMed2002

Relationship of body iron stores to levels of serum ferritin, serum iron, unsaturated iron binding capacity and transferrin saturation in patients with iron storage disease.

None of the methods for assessing total body iron burden in patients with hemochromatosis is satisfactory. Although it is commonly believed that a relationship exists between serum ferritin levels and total iron burden, the extent of this relationship has not previously been documented. In the present investigation we measured the total body iron burden of 88 patients with putative hemochromatosis, 54 of whom were homozygotes for the 845G-->A (C282Y) mutation. The total body iron stores were estimated from the volume of red cells removed during therapeutic phlebotomy corrected for an estimated 2 mg/day dietary iron absorbed during the phlebotomy period; the amount of storage iron was compared to the serum ferritin, serum iron, unsaturated iron binding capacity, and transferrin saturation before the beginning of phlebotomy. The serum ferritin proved to be the best predictor of body iron stores. The correlation between all of the analytes and the body iron burden was greater in patients homozygous for the C282Y mutation than in those who were not, including the compound heterozygotes for C282Y and H63D. The body iron burden tended to be greater in patients homozygous for the C282Y mutation than the other patients at any other given ferritin level. We conclude that the serum ferritin level does provide some information regarding total iron burden but even in the case of C282Y homozygotes, the correlation is not very strong.

Ferritins↗
PubMed2000

Involvement of iron (ferric) reduction in the iron absorption mechanism of a trivalent iron-protein complex (iron protein succinylate).

Iron protein succinylate is a non-toxic therapeutic iron compound. We set out to characterise the structure of this compound and investigate the importance of digestion and intestinal reduction in determining absorption of the compound. The structure of the compound was investigated by variable temperature Mössbauer spectroscopy, molecular size determinations and kinetics of iron release by chelators. Intestinal uptake was determined with radioactive compound force fed to mice. Reduction of the compound was determined by in vitro incubation with intestinal fragments. The compound was found to contain only ferric iron, present as small particles including sizes below 10 nm. The iron was released rapidly to chelators. Digestion with trypsin reduced the molecular size of the compound. Intestinal absorption of the compound was inhibited by a ferrous chelator (ferrozine), indicating that reduction to ferrous iron may be important for absorption. The native compound was a poor substrate for duodenal reduction activity, but digestion with pepsin, followed by pancreatin, released soluble iron complexes with an increased reduction rate. We conclude that iron protein succinylate is absorbed by a mechanism involving digestion to release soluble, available ferric species which may be reduced at the mucosal surface to provide ferrous iron for membrane transport into enterocytes.

Animals↗