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Biomedical subjects

Bo Lönnerdal

Publications and source records attributed to Bo Lönnerdal.

At least 37 records · Page 2Linked to original sources
PubMed2005

A follow-up study of nutrient intake, nutritional status, and growth in infants with cow milk allergy fed either a soy formula or an extensively hydrolyzed whey formula.

BACKGROUND: Infants with cow milk allergy (CMA) are reported to have reduced growth and special nutritional needs. OBJECTIVE: The aim of the present study was to compare nutrient intake, nutritional status, and growth in infants with CMA who were fed either a soy formula or an extensively hydrolyzed whey formula. DESIGN: The study group comprised 168 double-blind challenge-proven infants with CMA. Eighty-four of the infants were fed a soy formula (mean starting age: 7.8 mo), and the other 84 infants were fed an extensively hydrolyzed whey formula (mean starting age: 7.5 mo). RESULTS: The length (SD score) of the infants was close to the mean Finnish reference growth by age 2 y in both groups. Weight-for-length measurements continued to reach the 50th percentile by age 4 y in both study groups. The mean nutrient intake followed the recommended intake in both groups, although most of the infants were supplemented with calcium and vitamin D. The observed serum transferrin receptor concentrations indicated a greater iron inadequacy in the tissue of infants in the soy formula group than in the hydrolyzed whey formula group (P = 0.08). However, there were no significant differences between the groups either in the percentages of abnormally low laboratory values (mean cell volume, hemoglobin, zinc, and ferritin) or in the percentages of high alkaline phosphatase activity, which indicates the comparable safety and effectiveness of the formulas studied. CONCLUSIONS: Both nutritional status and growth were well within reference values in the 2 groups, and the selection of a formula can largely be made on the basis of infant tolerance to the formulas.

Child, Preschool↗
PubMed2005

Effects of chronic copper exposure during early life in rhesus monkeys.

BACKGROUND: Whether infants regulate copper absorption and the potential effects of excess copper in early life remain poorly defined. OBJECTIVE: The objective of the study was to assess copper retention, liver copper content, and liver function in infant rhesus monkeys fed infant formula containing 6.6 mg Cu/L. DESIGN: From birth to 5 mo of age, infant rhesus monkeys were fed formula that was supplemented with copper (0.6 mg Cu/L; n = 5) or not supplemented (n = 4). In all animals, weight and crown-rump length (by anthropometry), hemoglobin, hematocrit, plasma ceruloplasmin activity, and zinc and copper concentrations were measured monthly (birth to 6 mo) and at 8 and 12 mo. When the animals were 1, 5, and 8 mo old, liver copper and metallothionein concentrations, liver histology (by light and electron microscopy), and the number of Kupffer cells were assessed, and 67Cu retention was measured. Liver function was assessed by measurement of plasma alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, and alkaline phosphatase activities and protein, albumin, bilirubin, and blood urea nitrogen concentrations. RESULTS: 67Cu retention was 19.2% and 10.9% after 1 and 5 mo of copper treatment, respectively, compared with approximately 75% in controls at age 2 mo. At age 8 mo, 67Cu retention was 22.9% in copper-treated animals and 31.5% in controls. Liver histology remained normal by light microscopy, with mild ultrastructural signs of cell damage at 5 mo. Liver copper concentration was 4711, 1139, and 498 microg/g dry tissue at 1, 5, and 8 mo, respectively, in copper-treated animals and 250 microg/g at 2 mo in controls. Measurements could not be completed in all animals. CONCLUSIONS: No clinical evidence of copper toxicity was observed. Copper absorption was down-regulated; increases in liver copper content at ages 1 and 5 mo did not result in histologic damage. Ultrastructural changes at age 5 mo could signal early cellular damage.

Administration, Oral↗
PubMed2005

Anemia, iron deficiency, and iron deficiency anemia in 12-36-mo-old children from low-income families.

BACKGROUND: Iron deficiency (ID) is the most common nutritional deficiency in the world and remains relatively common in at-risk groups in the United States. The actual prevalence of anemia, ID, and iron deficiency anemia (IDA) in California remains unclear. OBJECTIVE: The objective was to determine the prevalence of anemia, low iron stores, ID, and IDA in children participating in the Special Supplemental Nutrition Program for Women, Infants and Children (WIC) population, and to assess the value of using hemoglobin to predict ID. DESIGN: This was a cross-sectional study of a convenience sample of 12-36-mo-old children from WIC clinics in 2 California counties. RESULTS: The prevalence of anemia was 11.1% (hemoglobin <110 g/L at 12-24 mo or <111 g/L at 24-36 mo). Study- and literature-determined abnormal values for iron measures were as follows: serum ferritin or=8.4 or >10.0 microg/mL, and transferrin saturation or=2 abnormal iron measures) were 16.2% and 8.8%, and of IDA (ID with low hemoglobin) were 3.4% and 3.2% on the basis of study- and literature-determined cutoffs, respectively. Hemoglobin concentration was used to predict study- and literature-determined ID on the basis of receiver operating characteristic curves. The sensitivity of low hemoglobin in predicting study- and literature-determined ID was low (23.2% and 40.0%, respectively). CONCLUSIONS: Anemia and ID were prevalent in this WIC sample, but IDA was uncommon. Low hemoglobin is a poor predictor of ID.

Anemia↗
PubMed2005

Low vitamin a intake affects milk iron level and iron transporters in rat mammary gland and liver.

Marginal vitamin A deficiency is common and can result in a secondary iron (Fe) deficiency. A positive correlation between maternal Fe status and milk Fe was observed in lactating women supplemented with both vitamin A and Fe but not with Fe alone, suggesting effects of vitamin A on mammary gland Fe transport. We hypothesized that low vitamin A intake during lactation elicits differential effects on mammary gland and liver Fe transport and storage proteins, thus affecting milk Fe concentration but not maternal Fe status. We fed rats a control (CON, 4 RE/g) or a marginal vitamin A diet (AD, 0.4 RE/g) through midlactation. Effects on plasma, milk, liver and mammary gland Fe and vitamin A concentrations, and divalent metal transporter-1 (DMT1), ferroportin (FPN), ferritin (Ft), and transferrin receptor (TfR) expression were determined. Dams fed AD were not vitamin A or Fe deficient. Milk and liver vitamin A and Fe and mammary gland Fe concentrations were lower in rats fed AD compared with rats fed CON. Liver TfR expression was higher, whereas mammary gland TfR expression was lower in rats fed AD compared with rats fed CON. Liver Ft was unaffected, whereas mammary gland Ft was lower in rats fed AD compared with rats fed CON. Liver and mammary gland DMT1 and FPN protein levels were lower in rats fed AD compared with rats fed CON. Our results indicate that the mammary gland and liver respond differently to marginal vitamin A intake during lactation and that milk Fe is significantly decreased due to effects on mammary gland Fe transporters, putting the nursing offspring at risk for Fe deficiency.

Animals↗
PubMed2005

Zinc deficiency is associated with increased brain zinc import and LIV-1 expression and decreased ZnT-1 expression in neonatal rats.

Zinc (Zn) deficiency has been associated with adverse behavioral outcomes in infants and children. However, Zn deficiency does not affect brain Zn concentration, suggesting that brain Zn homeostasis is tightly regulated. The recent identification of Zn-specific transport proteins allowed us to examine effects of low Zn intake on tissue Zn level, brain Zn uptake, and zinc transporter expression and localization in neonatal rat brain. Female rats were fed diets differing only in Zn content [7, moderately zinc deficient (ZD); 10, marginally zinc deficient (MZD); or 25 mg Zn/kg, control] and pups were killed on postnatal d 11. Plasma and brain Zn concentrations were measured, brain Zn uptake was assessed using (65)Zn, brain metallothionein-I and -III; LIV-1, zinc transporter ZnT-1, and ZnT-3 expression was measured by semiquantitative RT-PCR. LIV-1 localization in the brain was determined by immunohistochemistry; brain and hippocampi LIV-1 and ZnT-1 protein expressions were measured by Western blotting. Plasma Zn concentration was lower in MZD and ZD pups, whereas brain Zn concentration was not affected. Brain Zn uptake was higher in MZD and ZD rats compared with controls. Metallothionein-I and ZnT-1 expressions were lower and LIV-1 expression was higher in the whole brain of MZD and ZD pups. Metallothionein-III and ZnT-3 mRNA expressions were not affected. LIV-1 was localized to the plasma membrane of many brain cell types, including hippocampal pyramidal neurons and the apical membrane of the choroid plexus. Our results indicate that Zn deficiency results in alterations in Zn transporter expression, which facilitates increased brain Zn uptake and results in the conservation of brain Zn during Zn deficiency.

Animals↗
PubMed2005

A graded model of dietary zinc deficiency: effects on growth, insulin-like growth factor-I, and the glucose/insulin axis in weanling rats.

OBJECTIVE: Severe zinc (Zn) deficiency inhibits growth, insulin storage and release. Mild or moderate Zn deficiency may also have profound physiological effects that are not outwardly evident. We examined the effects of graded levels of low Zn intake on growth, insulin-like growth factor-I (IGF-I) and glucose homeostasis in weanling rats. METHODS: Weanling rats were fed ad libitum for 3 weeks with diets containing different Zn levels: very low Zn, low Zn or mildly low Zn; there was also a control group and an additional group was pair-fed to very low Zn rats. Growth and food intake were recorded. Serum Zn, IGF-I, IGF binding protein-3 (IGFBP-3), serum insulin and glucose, tissue Zn and jejunal sucrase activity were measured. Relative liver IGF-I and IGFBP-3 mRNA levels were quantified. RESULTS: Serum and tissue Zn were significantly lower in rats fed very low Zn (compared with pair-fed animals and controls) and low Zn (compared with controls). Growth was significantly lower in rats fed very low Zn and pair-fed animals (compared with controls) and in those fed very low Zn (compared with pair-fed animals). Liver IGF-I and IGFBP-3 mRNA levels were higher in low Zn animals compared with controls. Serum IGF-1 and IGFBP-3 levels were not affected by diet. Serum glucose was significantly higher in rats fed very low Zn than in pair-fed animals (191 +/- 28 vs 99 +/- 5 mg/dL, respectively). Sucrase activity was lower in rats fed very low Zn than in pair-fed animals or controls and a linear relationship was observed between serum glucose and insulin (r = 0.65, P < 0.01) in pair-fed animals and controls but not in Zn-deficient groups. CONCLUSION: Severe Zn deficiency was associated with hyperglycemia and relative hypoinsulinemia. Mild degrees of Zn deficiency also altered glucose metabolism, suggesting that Zn intake may be a sensitive regulator of glucose homeostasis.

Animals↗
PubMed2005

Maternal zinc deficiency reduces NMDA receptor expression in neonatal rat brain, which persists into early adulthood.

Prenatal and early postnatal zinc deficiency impairs learning and memory and these deficits persist into adulthood. A key modulator in this process may be the NMDA receptor; however, effects of zinc deficiency on the regulation of NMDA receptor activity are not well understood. Female Sprague-Dawley rats were fed diets containing 7 (zinc deficient, ZD), 10 (marginally zinc deficient, MZD) or 25 (control) mg Zn/g diet preconception through postnatal day (PN) 20, at which time pups were weaned onto their maternal or control diet. Regulation of NMDA receptor expression was examined at PN2, PN11, and PN65. At PN2, expression of whole brain NMDA receptor subunits NR1, NR2A, and NR2B was lower in pups from dams fed ZD and MZD compared to controls, as analyzed using relative RT-PCR and immunoblotting. At PN11, whole brain and hippocampi NR1, NR2A, NR2B and PSA-NCAM (polysialic acid-neural cell adhesion molecule) expression and the number of PSA-NCAM immunoreactive cells were lower in pups from dams fed ZD compared to controls. Whole brain brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) concentrations were lower in pups from dams fed ZD or both low zinc diets, respectively. Whole brain NR1 expression remained lower in previously zinc-deficient rats at PN65. These data indicate potential mechanisms through which developmental zinc deficiency can impair learning and memory later in life.

Animals↗
PubMed2004

Effects of copper supplementation on copper absorption, tissue distribution, and copper transporter expression in an infant rat model.

Infants are exposed to variable copper (Cu) intake; Cu in breast milk is low, whereas infant formulas vary in Cu content as well as the water used for their preparation. Little is known about the regulation of Cu absorption during infancy. The objectives of this study were to determine effects of Cu supplementation on Cu absorption and tissue distribution and the expression of Cu transporters in an infant rat model. Suckling rat pups were orally dosed with 0, 10, or 25 microg Cu/day. Intestine and liver were collected at days 10 and 20, and Cu concentration, Cu transporter-1 (Ctr1), Atp7A, Atp7B, and metallothionein (MT) mRNA and protein levels were measured. 67Cu absorption was measured at days 10 and 20. Total 67Cu absorption decreased, and intestinal 67Cu retention increased with increased Cu intake. At day 10, intestine Cu concentration, MT mRNA, and Ctr1 protein levels increased with supplementation, but no changes in Atp7A or Atp7B levels were observed. At day 20, intestine Cu concentration was unaffected by Cu supplementation, but Ctr1 protein and Atp7A mRNA and protein levels were higher than in controls. In liver, Cu level reflected Cu intake at days 10 and 20. There was a significant increase in Ctr1, Atp7B, and MT mRNA expression in liver at both ages with Cu supplementation. In conclusion, the ability of suckling rat pups to tolerate varying amounts of dietary Cu may be due to changes in Cu transporters, facilitated by transcriptional and posttranslational mechanisms. Despite these adaptive changes, Cu supplementation resulted in elevated alanine aminotransferase levels, suggesting a risk of Cu toxicity with supplementation during infancy.

Animals↗
PubMed2004

Functional and molecular responses of suckling rat pups and human intestinal Caco-2 cells to copper treatment.

Ctr1 and Atp7A are copper (Cu) transporters that may play a role in the regulation of intestinal Cu absorption; however, intestinal regulation of these transporters by Cu in vivo has not been well defined. In this study, we hypothesized that Cu supplementation would alter the expression of intestine Ctr1 and Atp7A in vivo and further documented effects of Cu exposure on Cu transport, Ctr1 and Atp7A levels and localization in enterocyte-like Caco-2 cells. Suckling rat pups were supplemented with Cu (0 and 25 microg Cu/day) for 10 days and small intestine Cu concentration, Ctr1, Atp7A and metallothionein (MT) gene expression were measured by Northern blot analysis. Caco-2 cells were treated with basal medium, or medium supplemented with 3 and 94 microM CuSO4 and 67Cu transport, Ctr1 and Atp7A levels and localization were determined. In rat pups, Cu supplementation increased intestinal Cu, Ctr1 and MT gene expression; however, Atp7A gene expression was not significantly affected. Caco-2 cells treated with 94 microM Cu had lower cellular Cu uptake and export compared to untreated cells. While Ctr1 and Atp7A gene and protein levels were unaffected, confocal microscopy indicated that Ctr1 was endocytosed and co-localized with transferrin in Cu treated cells. This study demonstrates the functional response of intestinal cells to Cu treatment and suggests that both Ctr1 and Atp7A may regulate Cu absorption.

Absorption↗
PubMed2004

Baculovirus expression of mouse lactoferrin receptor and tissue distribution in the mouse.

Lactoferrin (Lf) has been shown to have a role in the immune system and in early development of the mouse embryo. A specific receptor for Lf has been suggested to mediate the functions of Lf. We have recently identified a Lf receptor (LfR) in human fetal small intestine. We therefore hypothesized that the mouse homologue of this protein functions as a LfR. We expressed mouse Lf (MLf) and the mouse homologue (MLfR) in a baculovirus-insect cell system. The recombinant MLfR (rMLfR) was purified by immobilized recombinant MLf (rMLf) affinity chromatography, demonstrating an interaction between rMLf and the rMLfR. RT-PCR revealed that MLfR was expressed in various tissues and during embryonic development. Immunohistochemical analysis revealed that the MLfR was localized in various tissues including small intestinal epithelium, stomach, kidney, ovary, and various regions of brain. In summary, the MLfR functions as a receptor for MLf, is expressed and localized in various tissues, and may be involved in the indispensable function of MLf during early embryonic development.

Animals↗
PubMed2004

Cellular internalization of lactoferrin in intestinal epithelial cells.

We studied the cellular internalization of lactoferrin (Lf) in an intestinal epithelial cell line, Caco-2, to investigate the mechanism of biological actions of ingested Lf. RT-PCR and Western blotting analyses revealed that differentiated Caco-2 cells express LfR mRNA and its protein with a 34 kD molecular weight under reducing conditions. Biotin-labeled Lf showed specific binding to the cellular membrane of differentiated Caco-2 cells with a dissociation constant (Kd) of 0.16 microM. The cellular internalization of Lf was studied in differentiated Caco-2 cells grown as monolayers on Transwell inserts, and compared to that of human transferrin (Tf). After labeling with fluorescent dye, either Lf or Tf was added to Caco-2 cells from the apical side or the basolateral one. Laser scanning confocal microscopy showed that labeled Lf was internalized only from the apical side and localized to the nuclei. On the other hand, labeled Tf was internalized from the basolateral side, not from the apical side, and localized in the cytoplasm. The internalization of labeled Lf was inhibited by excess of unlabeled Lf, but not of Tf. The internalization of labeled Lf, but not of labeled Tf, was also suppressed by heparin. This indicates that a heparin-binding site in the N-terminal region of Lf could be important for the internalization of Lf. These findings suggest that ingested Lf might be internalized by the intestinal epithelium in a manner different from Tf and might function in the nucleus.

Animals↗
PubMed2004

Iron, zinc, and copper concentrations in breast milk are independent of maternal mineral status.

BACKGROUND: Little is known about the regulation of iron, zinc, and copper in breast milk and the transport of these minerals across the mammary gland epithelium. OBJECTIVE: The objective was to study associations between breast-milk concentrations of iron, zinc, and copper and maternal mineral status. DESIGN: Milk samples from 191 Swedish and Honduran mothers were collected at 9 mo postpartum. Iron, zinc, and copper concentrations were measured by atomic absorption spectrometry. Blood samples from mothers were analyzed for plasma zinc and copper and 4 indexes of iron status: hemoglobin, plasma ferritin, soluble transferrin receptors, and zinc protoporphyrin. Complementary food energy (CFE) intake was used as an inverse proxy for breast-milk intake. RESULTS: Mean (+/-SD) breast-milk concentrations of iron were lower in the Honduran than in the Swedish mothers (0.21 +/- 0.25 compared with 0.29 +/- 0.21 mg/L; P < 0.001), and mean breast-milk concentrations of zinc and copper were higher in the Honduran than in the Swedish mothers [0.70 +/- 0.18 compared with 0.46 +/- 0.26 mg/L (P < 0.001) and 0.16 +/- 0.21 compared with 0.12 +/- 0.22 mg/L (P = 0.001), respectively]. Milk iron was positively correlated with CFE intake (r = 0.24, P = 0.001) but was not significantly correlated with any iron-status variable. Milk zinc was negatively correlated with CFE intake (r = -0.24, P = 0.001) but was not significantly correlated with maternal plasma zinc. Milk copper was not significantly correlated with CFE intake or maternal plasma copper. CONCLUSIONS: Milk iron, zinc, and copper concentrations at 9 mo postpartum are not associated with maternal mineral status, which suggests active transport mechanisms in the mammary gland for all 3 minerals. Milk iron concentrations increase and milk zinc concentrations decrease during weaning [corrected]

Adult↗
PubMed2004

Effect of a micronutrient fortificant mixture and 2 amounts of calcium on iron and zinc absorption from a processed food supplement.

BACKGROUND: Iron, zinc, and calcium can interact with each other in a way that inhibits their respective absorption. On the other hand, mineral fortification has been used to improve simultaneous iron and zinc absorption from food supplements. OBJECTIVE: We evaluated the effect of a novel fortificant mixture consisting of NaFeEDTA, zinc methionine, ascorbic acid, and citric acid on iron and zinc absorption from a dry food supplement designed for preschool children. DESIGN: The standard food supplement contained cereal and legume flour, dried milk, and a mixture of micronutrients including ferrous sulfate and zinc sulfate as sources of supplemental iron and zinc, respectively. Standard and novel food products were prepared as porridge with or without the addition of 200 mg Ca as calcium phosphate. Iron absorption and zinc absorption from the food products were evaluated simultaneously in 13 nonpregnant, adult women by extrinsically labeling the products with radioisotopes of iron and zinc and carrying out whole-body counting 7 d after the food products were consumed in random order. RESULTS: The absorption of iron from the NaFeEDTA-containing (novel) food product was 1.7 times that from the ferrous sulfate-containing (standard) product (P = 0.015). There was no significant effect of dietary calcium on iron absorption. Zinc absorption was not associated with the form of zinc consumed, but higher dietary calcium was marginally associated with lower zinc absorption (P = 0.071). CONCLUSIONS: A mixture of fortificants containing NaFeEDTA, zinc sulfate or zinc methionine, ascorbic acid, and citric acid, but without calcium, can improve iron and zinc absorption from food products. A cost-benefit analysis of the novel fortificant mixture needs to be performed.

Adult↗
PubMed2004

Randomized controlled trial of the effect of daily supplementation with zinc or multiple micronutrients on the morbidity, growth, and micronutrient status of young Peruvian children.

BACKGROUND: Zinc supplements reduce childhood morbidity in populations in whom zinc deficiency is common. In such populations, deficiencies in other micronutrients may also occur. OBJECTIVE: The objective was to determine whether the administration of other micronutrients with zinc modifies the effect of zinc supplementation on children's morbidity and physical growth. DESIGN: Two hundred forty-six children aged 6-35 mo with persistent diarrhea were randomly assigned to 1 of 3 groups to receive a daily supplement of 10 mg Zn alone (Zn; n = 81), zinc plus vitamins and other minerals at 1-2 times recommended daily intakes (Zn+VM; n = 82), or placebo (n = 83) for approximately 6 mo after the diarrhea episode ended. Morbidity information was collected on weekdays. Weight, length, and other anthropometric indicators were measured monthly, and plasma zinc and other indicators of micronutrient status were measured at baseline and 6 mo. RESULTS: Supplement consumption was high ( approximately 90%) in all groups, although slightly more vomiting was reported in the Zn+VM group (P < 0.0001, analysis of variance). The change in plasma zinc from baseline to 6 mo was greater in the 2 zinc groups (6.1, 27.3, and 16.2 micro g/dL in the placebo, Zn, and Zn+VM groups, respectively; P < 0.0001, analysis of variance). The Zn group had fewer episodes of diarrhea, dysentery, and respiratory illness and a lower prevalence of fever and cough than did the Zn+VM group and a lower prevalence of cough than did the placebo group (P = 0.05). No significant effects of supplementation on growth were observed. CONCLUSION: Morbidity was greater after supplementation with zinc plus multivitamins and minerals than it was after supplementation with zinc alone.

Anthropometry↗
PubMed2004

A community-based randomized controlled trial of iron and zinc supplementation in Indonesian infants: effects on growth and development.

BACKGROUND: Deficiencies of iron and zinc are associated with delayed development, growth faltering, and increased infectious-disease morbidity during infancy and childhood. Combined iron and zinc supplementation may therefore be a logical preventive strategy. OBJECTIVE: The objective of the study was to compare the effects of combined iron and zinc supplementation in infancy with the effects of iron and zinc as single micronutrients on growth, psychomotor development, and incidence of infectious disease. DESIGN: Indonesian infants (n = 680) were randomly assigned to daily supplementation with 10 mg Fe (Fe group), 10 mg Zn (Zn group), 10 mg Fe and 10 mg Zn (Fe+Zn group), or placebo from 6 to 12 mo of age. Anthropometric indexes, developmental indexes (Bayley Scales of Infant Development; BSID), and morbidity were recorded. RESULTS: At 12 mo, two-factor analysis of variance showed a significant interaction between iron and zinc for weight-for-age z score, knee-heel length, and BSID psychomotor development. Weight-for-age z score was higher in the Zn group than in the placebo and Fe+Zn groups, knee-heel length was higher in the Zn and Fe groups than in the placebo group, and the BSID psychomotor development index was higher in the Fe group than in the placebo group. No significant effect on morbidity was found. CONCLUSIONS: Single supplementation with zinc significantly improved growth, and single supplementation with iron significantly improved growth and psychomotor development, but combined supplementation with iron and zinc had no significant effect on growth or development. Combined, simultaneous supplementation with iron and zinc to infants cannot be routinely recommended at the iron-to-zinc ratio used in this study.

Anemia, Iron-Deficiency↗
PubMed2004

Iron in ferritin or in salts (ferrous sulfate) is equally bioavailable in nonanemic women.

BACKGROUND: Recent studies in humans suggest that ferritin iron in soybeans has high bioavailability. However, direct evidence for this is lacking because the soybeans were intrinsically labeled; thus, iron bound to other ligands, such as phytate, was also labeled. OBJECTIVE: The objectives of the study were to evaluate the absorption of iron from extrinsically labeled, purified ferritin (horse spleen) reconstituted with either high-phosphate iron mineral (plant-type) or low-phosphate iron mineral (animal-type) and to compare it with iron absorption from ferrous sulfate. DESIGN: Nonanemic, healthy young women were fed a standard breakfast meal supplemented with (59)Fe-labeled ferritin or ferrous sulfate, in randomized order. Fifteen subjects received ferritin with the low-phosphate iron mineral, and 15 subjects received ferritin with the high-phosphate iron mineral. Iron absorption was measured in a whole-body counter after 14 and 28 d and by red blood cell incorporation after 28 d. RESULTS: There was no significant difference in iron absorption between ferritin and ferrous sulfate: low-phosphate iron mineral ferritin (x +/- SD: 21.4 +/- 14.7%) compared with ferrous sulfate (21.9 +/- 14.6%), or high-phosphate iron mineral ferritin (22.2 +/- 19.2%) compared with ferrous sulfate (16.7 +/- 7.1%). Results obtained by using whole-body retention of iron and red blood cell incorporation differed with the type of iron, which suggests that pathways for iron uptake and utilization differed for the 2 forms. CONCLUSIONS: Iron is equally well absorbed from ferritin and ferrous sulfate independent of the phosphate content of the ferritin iron mineral. Thus, dietary ferritin iron is likely to be a good source of iron.

Analysis of Variance↗