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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In Sweden a multicentre nutritional survey was performed in 1980-81 in four different parts of Sweden. The total number of children investigated was 1109, of whom 92 were two years old, 332 four years, 338 eight years and 347 thirteen years. The 24-hour recall method was used in all children. In addition 7-day record was used in the 2-, 4- and 8-year-olds and the dietary history method in the 13-year-olds. During the weekdays the 2-, 4-, 8- and 13-year-old children had 5.9, 5.8, 5.4 and 5.2 meals and snacks per day, respectively. During weekends these respective numbers decreased to 5.7, 5.6, 5.1 and 5.0. The mean number of light meals and snacks was almost the same on all days and varied between 2.4 and 3.3 in the different age groups. The part of the energy intake deriving from snacks has increased during the last 15 years. The mean daily energy intakes for the 2-, 4-, 8- and 13-year-old boys and girls were 5.8 and 5.6, 6.9 and 6.5, 8.9 and 7.9 and 12.1 and 9.7 MJ respectively. These values are below the recommendations for all age groups except the 2-year-old boys. The mean daily intakes of protein, retinol, ascorbic acid, thiamin, riboflavin, niacin, vitamin B12 and calcium were almost invariably higher or much higher than the recommendations, while those of vitamin D and zinc were below the recommended values. The iron intake fulfilled the recommendations except for the 2-year-olds and the 13-year-old girls. The intake of protein and fat expressed in per cent of the total energy intake was very similar in all age groups, about 14 per cent and 35-37 per cent respectively. The mean ratio between polyunsaturated and saturated fatty acids (P/S ratio) was also the same in all age groups, i.e. 0.22-0.23. This low ratio is explained by a high consumption of dairy products. Furthermore, the nutrient density of the food did not change appreciably with age. The only exception was found for the 2-year-old children, who had slightly higher nutrient density values on account of a relatively high consumption of fortified follow-up formula. In all age groups the mean nutrient densities of vitamins D and B6 and of iron were below the recommendations to varying degrees. No clinical signs of nutritional deficiencies, iron deficiency included, were found in any age group.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Food habits and nutrient intake in childhood in relation to health and socio-economic conditions. A Swedish Multicentre Study 1980-81. 347 Oct 46

A 32-mo-long, double-blind field study involving one highland control community receiving only vitamin A-fortified sugar and three vitamin A- and FeNaEDTA-sugar-fortified communities, two in the lowlands and one in the highlands of Guatemala, was undertaken to test the effectiveness of this approach in controlling iron deficiency. The communities' population ranged between 1200 and 17000. Sugar fortified with 1 g FeNaEDTA and 15 mg retinol as retinyl palmitate/kg was stable, did not segregate, and was well accepted by the communities. The impact of fortification on iron nutrition was estimated at 8, 20, and 32 mo of intervention. All pregnant women and subjects with severe anemia received supplements or treatment and were excluded from the analysis. Iron stores in the fortified communities increased significantly except for women 18-48 y of age in one lowland community and > 49 y in the highland community. Iron stores in the control community remained unchanged except for a rise among adult males.
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PMID:Fortification of sugar with iron sodium ethylenediaminotetraacetate (FeNaEDTA) improves iron status in semirural Guatemalan populations. 859 28

Nutritional anaemia, thought to be caused by iron deficiency, affects 50-70% of pregnant women in the developing world. The influence of vitamin A and iron supplementation was studied in anaemic pregnant women in West Java, in a randomised, double-masked, placebo-controlled field trial. 251 women aged 17-35 years, parity 0-4, gestation 16-24 weeks, and haemoglobin between 80 and 109 g/L were randomly allocated to four groups: vitamin A (2.4 mg retinol) and placebo iron tablets; iron (60 mg elemental iron) and placebo vitamin A; vitamin A and iron; or both placebos, all daily for 8 weeks. Maximum haemoglobin was achieved with both vitamin A and iron supplementation (12.78 g/L, 95% Cl 10.86 to 14.70), with one-third of the response attributable to vitamin A (3.68 g/L, 2.03 to 5.33) and two-thirds to iron (7.71 g/L, 5.97 to 9.45). After supplementation, the proportion of women who became non-anaemic was 35% in the vitamin-A-supplemented group, 68% in the iron-supplemented group, 97% in the group supplemented with both, and 16% in the placebo group. Improvement in vitamin A status may contribute to the control of anaemic pregnant women.
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PMID:Supplementation with vitamin A and iron for nutritional anaemia in pregnant women in West Java, Indonesia. 790 29

We determined the influence of undernutrition on blood soluble transferrin receptor (sTfR) concentrations, an indicator of iron deficiency, in 99 Zairean women (aged 16-45 y) without inflammation. They were recruited during a survey on iron deficiency in rural Bas-Zaire. sTfR was measured by enzyme immunoassay, and indicators of nutritional status [albumin, transthyretin (or prealbumin), and retinol binding protein] were measured by radial immunodiffusion. Undernutrition was diagnosed if the concentration of any one of the indicators was below normal: albumin < 35 g/L, transthyretin < 160 mg/L, and retinol binding protein < 30 mg/L. The sTfR concentration ranged from 1.89 to 19.1 mg/L (mean: 8.7 mg/L). Mean values for indicators of nutritional status, serum ferritin, and transferrin saturation were within the normal range for health subjects. Regardless of the iron status (iron sufficiency, anemia, or iron deficiency with or without anemia) and whether women were pregnant or nonpregnant, undernutrition did not significantly reduce sTfR concentrations. A higher percentage (80%) of iron-deficient women with two or three protein values below normal had sTfR concentrations > 8 mg/L (which are suggestive of iron-deficiency erythropoiesis) compared with iron-deficient women with no (72.7%) or one (66.7%) protein value below normal, anemic women (46-60%) and iron-sufficient women (18.2-36.8%). Results suggest that sTfR can be used as an indicator of iron deficiency in field studies without in-depth assessment of nutritional status. However, the effect of severe malnutrition on this index requires further investigation.
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PMID:Serum transferrin receptor concentrations in women with mild malnutrition. 859 25

Iron regulatory protein 1 (IRP1) and IRP2 are cytoplasmic RNA binding proteins that are central regulators of mammalian iron homeostasis. We investigated the time-dependent effect of dietary iron deficiency on liver IRP activity in relation to the abundance of ferritin and the iron-sulfur protein mitochondrial aconitase (m-acon), which are targets of IRP action. Rats were fed a diet containing 2 or 34 mg iron/kg diet for 1-28 d. Liver IRP activity increased rapidly in rats fed the iron-deficient diet with IRP1 stimulated by d 1 and IRP2 by d 2. The maximal activation of IRP2 was five-fold (d 7) and three-fold (d 4) for IRP1. By d 4, liver ferritin subunits were undetectable and m-acon abundance eventually fell by 50% (P < 0.05) in iron-deficient rats. m-Acon abundance declined most rapidly from d 1 to 11 and in a manner that was suggestive of a cause and effect type of relationship between IRP activity and m-acon abundance. In liver, iron deficiency did not decrease the activity of cytosolic aconitase, catalase or complex I of the electron transport chain nor was there an effect on the maximal rate of mitochondrial oxygen consumption with the use of malate and pyruvate as substrates. Thus, the decline in m-acon abundance in iron deficiency is not reflective of a global decrease in liver iron-sulfur proteins nor does it appear to limit ATP production. Our results suggest a novel role for m-acon in cellular iron metabolism. We conclude that, in liver, iron deficiency preferentially affects the activities of IRPs and the targets of IRP action.
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PMID:Dietary iron intake rapidly influences iron regulatory proteins, ferritin subunits and mitochondrial aconitase in rat liver. 948 59

After the rapid decrease in the prevalence of iron deficiency and iron-deficiency anemia in the Venezuelan population when a national program for fortification of flours with iron and vitamins was instituted, we studied micronutrient interactions in Venezuelan diets. One hundred human adults were fed three cereal-based diets, labelled with either 59Fe or 55Fe in six studies. Each diet contained different concentrations of vitamin A (from 0.37 to 2.78 micromol/100 g cereal) or beta-carotene (from 0.58 to 2.06 micromol/100 g cereal). The presence of vitamin A increased iron absorption up to twofold for rice, 0.8-fold for wheat and 1.4-fold for corn. beta-carotene increased absorption more than threefold for rice and 1.8-fold for wheat and corn, suggesting that both compounds prevented the inhibitory effect of phytates on iron absorption. Increasing the doses of vitamin A or beta-carotene did not further significantly increase iron absorption. We measured the iron remaining in solution performing in vitro studies in which the pH of solutions was adjusted from 2 to 6 in the presence of vitamin A or beta-carotene. All of the iron from ferrous fumarate was soluble after changing the pH of the solution containing 3.4 micromol of beta-carotene to 6.0. Vitamin A was less effective. However, 78 +/- 18% of iron was soluble in the presence of 3.3 micromol of vitamin A, whereas with no vitamin addition, only 26 +/- 13% of iron was soluble (<0.05). Vitamin A and beta-carotene may form a complex with iron, keeping it soluble in the intestinal lumen and preventing the inhibitory effect of phytates and polyphenols on iron absorption.
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PMID:Vitamin A and beta-carotene can improve nonheme iron absorption from rice, wheat and corn by humans. 948 76

We assessed whether iron deficiency alters the concentration of vitamin A (VA) in plasma or liver and the chemical distribution between hepatic unesterified and esterified retinol. Weanling male Sprague-Dawley rats (n = 10/group) were allocated to one of four diet groups: low iron (ID3, 3 mg of elemental iron/kg diet), marginal iron (ID15, 15 mg/kg), control diet food-restricted to the ID3 group (FR, 35 mg/kg), and control diet ad libitum consumption (AD, 35 mg/kg). Both ID3 and FR rats grew less than AD and ID15 rats. At the end of 5.5 wk, plasma retinol concentrations of the ID3 and FR rats were reduced >40% compared to ID15 and AD rats [Kruskal-Wallis test (K-W), P < 0.0042)]. Paradoxically, the hepatic VA concentration was greater in FR rats, with accumulation of more retinyl esters and retinol compared to the other dietary groups. Concentrations of hepatic retinyl esters and retinol did not differ among the other groups, but the molar ratio of hepatic retinyl esters to retinol was greater in ID3 rats (20.1 +/- 1.4) compared to ID15 rats (13.8 +/- 1.6, P = 0.02), AD (11.3 +/- 2.1, P < 0.0042) and FR (9.5 +/- 1.1, P < 0.0042). Iron deficiency may cause changes in liver and plasma VA that are refractory to VA intake, and thus a benefit may be derived from combining iron and VA supplements during nutrition interventions.
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PMID:Iron deficiency in young rats alters the distribution of vitamin A between plasma and liver and between hepatic retinol and retinyl esters. 1035 91

A National fortification program instituted in Venezuela in 1993 reduced iron deficiency and anemia by half in only 1 y. The fortification mixture contained ferrous fumarate, vitamin A and other vitamins. We conducted experiments to characterize ferrous fumarate uptake by Caco-2 cells. Increasing amounts of ferrous fumarate, vitamin A, phytate, tannic acid and beta-carotene were added to incubation mixtures using a range of concentrations that included the molar ratios used in the Venezuelan fortification program. Cells were incubated for 1 h at 37 degrees C with 37 kBq (59)Fe and the compound to be evaluated. They were then rinsed, trypsinized and counted to measure uptake. Effects of ascorbic acid, days in culture and use of flasks or inserts were also evaluated. Optimal conditions for uptake experiments were pH 5.5, in the presence of ascorbic acid and at 16 d in culture. Use of flasks or inserts did not affect uptake. Vitamin A did not significantly increase iron uptake under the experimental conditions employed. However, beta-carotene (6 micromol/L) significantly increased iron uptake compared to no beta-carotene addition (114.9 +/- 6.3 and 47.2 +/- 5.9 pmol/mg cell protein, respectively). Moreover, in the presence of phytates or tannic acid, beta-carotene generally overcame the inhibitory effects of both compounds depending on their concentrations. We conclude that beta-carotene improves iron uptake and overcomes the inhibition by potent inhibitors of iron absorption. These experiments also validated the usefulness of Caco-2 cell model system to evaluate iron metabolism.
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PMID:Beta-carotene and inhibitors of iron absorption modify iron uptake by Caco-2 cells. 1061 57

In view of evidence that nutritional status of iron and vitamin A may affect the other nutrient's metabolism, we used model-based compartmental analysis to examine effects of iron deficiency on whole-body vitamin A dynamics in rats. Weanling male Sprague-Dawley rats were fed the AIN93G diet with 2.5 nmol retinyl palmitate/g and either 45 [control (CN)] or 4 microg/g Fe [iron-deficient (ID)] for 8 wk. ID rats consumed food ad libitum; CN rats were food-restricted so that their body weights were the same as ID rats. Two rats/group were killed; liver vitamin A was determined and used for vitamin A balance calculations. [(3)H]Retinol-labeled plasma was administered intravenously to remaining rats, and 27 serial blood samples were collected for 7 wk. At killing, plasma vitamin A was 0.52+/-0.12 (ID, n = 5) vs. 1.34+/-0.12 micromol/L (CN, n = 6; P<0.001), and liver vitamin A was 809+/-94 (ID) vs. 112+/-24 nmol (CN, P<0.001). Plasma tracer data were fit to a three- or four-compartment model using the Simulation, Analysis and Modeling computer program and kinetic parameters were calculated. Vitamin A transfer rate between the retinyl ester storage pool [14+/-3 (ID) vs. 24+/-4 nmol/d (CN), P<0.05] and plasma was lower in ID rats. Vitamin A remained longer in the body [44+/-11 (ID) vs. 22+/-3 d (CN), P<0.05]. Adjusted mean disposal rate was lower in ID (10.0) than CN rats (19.9 nmol/d), as was estimated vitamin A absorption efficiency [58% (ID) vs. 76% (CN)]. Our results suggest that iron deficiency inhibits mobilization of vitamin A stores and may decrease the absorption and irreversible utilization of vitamin A.
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PMID:Kinetic analysis shows that iron deficiency decreases liver vitamin A mobilization in rats. 1080 32

Vitamin A deficiency produces anemia and altered iron status. In this study with rats we tested two hypotheses regarding vitamin A deficiency: (1) that it impairs erythropoiesis, leading to an increased red cell turnover, and (2) that it inhibits the glycosylation of transferrin. Erythropoietic activity was assessed indirectly by determining the myeloid:erythroid ratio in bone marrow smears, the number of erythroid colonies in the red pulp of spleen, the blood reticulocyte index, and zinc protoporphyrin and plasma transferrin receptor concentrations. Transferrin glycosylation was assessed by measuring the sialic acid content of transferrin. The effects of vitamin A deficiency were compared with those of iron deficiency. Iron deficiency produced anemia and low iron levels in organs. Vitamin A deficiency produced low levels of plasma and hepatic retinol, and it induced decreased plasma total iron-binding capacity and raised iron levels in tibia and spleen. Short- but not long-term iron deficiency reduced the number of erythroid colonies in spleen; vitamin A deficiency had no influence. Neither iron nor vitamin A deficiency influenced the myeloid:erythroid ratio in bone marrow smears and the blood reticulocyte production. Plasma transferrin receptor and erythrocyte zinc protoporphyrin concentrations were not affected by vitamin A deficiency but increased with iron deficiency. Vitamin A deficiency did not stimulate erythrocyte breakdown, as indicated by unaltered plasma lactate dehydrogenase activity and reduced plasma total bilirubin levels. Both vitamin A and iron deficiencies raised the proportion of multiple sialylated transferrins in plasma. Thus, we have not found evidence that vitamin A deficiency affects erythropoiesis and erythrocyte turnover. The iron accumulation in spleen and bone marrow may be related to reduced iron transport due to inhibition of transferrin synthesis rather than inhibition of transferrin sialylation.
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PMID:Indicators of erythrocyte formation and degradation in rats with either vitamin A or iron deficiency. 1082 45


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