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Bo Lönnerdal

Publications and source records attributed to Bo Lönnerdal.

76 records · Page 5Linked to original sources

Characterization of mammalian receptors for lactoferrin.

Lactoferrin (Lf) has been suggested to have several physiological functions. Specific binding of Lf, indicating the presence of Lf receptors (LfRs), has been observed in various types of mammalian cells such as lymphocytes, hepatocytes, and enterocytes. These LfRs are considered to function as a mediator for some of the functions of Lf. We here review current knowledge of mammalian LfRs characterized in different tissues. We also briefly present evidence for the existence of an LfR provided by our cloning of a human intestinal LfR (HLfR). The entire coding region of the HLfR was cloned by polymerase chain reaction (PCR), and a recombinant HLfR (rHLfR) was expressed in a baculovirus system. The rHLfR was purified by immobilized human Lf (HLf) affinity chromatography, indicating that the rHLfR retained the capacity to bind HLf. The gene was expressed at high levels in fetal small intestine and in adult heart but at lower levels in Caco-2 cells. In summary, we demonstrate the presence of a unique receptor-mediated mechanism for Lf, functioning in the small intestine of the newborn infant and possibly in other tissues of human adults.

Animals↗

High specific activity heme-Fe and its application for studying heme-Fe metabolism in Caco-2 cell monolayers.

Heme-Fe is an important source of dietary iron in humans. Caco-2 cells have been used extensively to study human iron absorption with an emphasis on factors affecting nonheme iron absorption. Therefore, we examined several factors known to affect heme iron absorption. Cells grown in bicameral chambers were incubated with high specific activity [59Fe]heme alone or with 1% globin, BSA, or fatty acid-free BSA (BSA-FA) to examine the effect of protein source on absorption. Heme iron absorption was enhanced by globin and inhibited by BSA and BSA-FA. Absorption of heme iron in cells pretreated for 7 days with serum-free medium containing 1, 25, 50, or 100 microM Fe was higher in the 1-microM-Fe pretreatment group than in all other groups (P < 0.05), showing an effect of iron status. Increased heme concentrations resulted in decreased percent absorbed but increased total heme iron absorption and increased transport rate across the basolateral membrane. Finally, cells treated with 10 microM CdCl2, which induces heme oxygenase, demonstrated higher absorption of [59Fe]heme than control cells (P < 0.05). Our results from Caco-2 cells are in agreement with human studies and make this a promising model for examining intestinal heme iron absorption.

Absorption↗

Sex differences in iron status during infancy.

BACKGROUND: It is commonly assumed that there is no difference in iron status between male and female infants, despite a lack of studies addressing this question. OBJECTIVE: To study sex differences in different measures of iron status in infants. METHODS: At 4 months of age, 263 term, breastfed infants (121 Swedish and 142 Honduran) were randomized to receive iron supplements or placebo until 9 months of age. Blood samples at 4, 6, and 9 months of age were analyzed for hemoglobin (Hb), mean cell volume (MCV), zinc protoporphyrin (ZPP), plasma ferritin, and transferrin receptors (TfR). RESULTS: At 4, 6, and 9 months, boys had significantly lower Hb, MCV, and ferritin and higher ZPP and TfR than girls. At 9 months, boys had a 10-fold higher risk of being classified as having iron deficiency anemia. The differences at 9 months in MCV (71.6 vs 75.1 fL) and ZPP (59 vs 49 micro mol/mol heme) remained significant after controlling for iron supplementation, site, growth variables, and other possible confounders. For ferritin, there was a remaining sex difference at 9 months among Swedish (29 vs 53 micro g/L) but not Honduran infants. For Hb and TfR, sex differences at 9 months were larger in unsupplemented infants, especially in those with a birth weight of <3500 g. CONCLUSIONS: There are substantial sex differences in Hb and other indicators of iron status during infancy. Some of these may be genetically determined, whereas others seem to reflect an increased incidence of true iron deficiency in boys.

Anemia, Iron-Deficiency↗

Molecular regulation of milk trace mineral homeostasis.

The regulation of milk trace mineral homeostasis requires the temporal integration of three main processes, (A) mineral uptake into the secretory mammary epithelial cell (MEC); followed by (B) mineral secretion from MEC into the alveoli lumen of the mammary gland for sequestration in milk; and then (C) milk release in response to suckling. Trace mineral requirements of term infants are generally met by exclusive breast-feeding through about the first 6 months of life and although milk zinc (Zn), iron (Fe), and copper (Cu) concentrations are relatively refractory to maternal trace mineral status, they normally decline throughout lactation. Recently, Zn-, Fe- and Cu-specific transporters have been identified that regulate trace element uptake and efflux in various cell types; however, there is currently little information available regarding the processes through which the mammary gland regulates milk trace mineral transport. The homology of trace mineral transporters between species permits the utilization of rodent models to examine the regulation of mammary gland mineral transport. Therefore, we have used the lactating rat to determine changes in mammary gland Zn, Fe and Cu transporter expression and localization that occur throughout lactation and in response to maternal trace mineral deficiency in hope of elucidating some of the changes which occur during mammary gland trace element homeostasis and also may be occurring in lactating women.

Animals↗