One hundred four infants were randomly assigned to receive whole cow milk plus iron-fortified cereal (WCM + C) in accord with the previous recommendations of the Committee of Nutrition/American Academy of Pediatrics (CON/AAP); one of two iron-fortified, follow-up formulas; or an iron-fortified infant formula. Mean iron intakes and vitamin C exceeded the recommended dietary allowance in all groups. By 12 mo of age, mean ferritin and mean corpuscular volume were lower in the WCM + C group and significantly more infants had serum ferritin concentrations < 12 micrograms/L. We conclude that infants 6-12 mo of age fed whole cow milk and iron-containing table food are at risk of developing depleted iron stores but not anemia. The iron insufficiency in these infants is not due to inadequate intake of iron or vitamin C, but probably to relatively poor bioavailability of iron in infant cereal.
Iron deficiency impairs lymphocyte proliferation in humans and laboratory animals by unknown mechanisms. In this study, we investigated whether this alteration can be attributed in part to impaired hydrolysis of cell membrane phosphatidyl inositol-4, 5-bisphosphate (PIP2), a required early event of T-lymphocyte activation. The study involved 46 iron-deficient (ID), 26 control (C) and 23 pair-fed (PF) mice, and ID mice that were repleted for 3 (n = 16), 7 (n = 17) or 14 d (n = 18). Mice were killed after 40-63 d (mean, 48 d) of consuming the test diet (0.09 mmol/kg iron) or the control diet (0.9 mmol/kg). The mean (+/-SEM) hemoglobin concentrations were 57 +/- 16.7, 176 +/- 2.6 and 181 +/- 9.7 g/L for ID, C and PF groups, respectively. After splenic lymphocytes were labeled in vitro with 3H-myoinositol for 3 h, PIP2 hydrolysis was estimated by measuring the radioactivity recovered as a mixture of inositol mono-, di- and triphosphate (IP) from concanavalin A (0, 1, 2.5, 5 and 10 mg/L) activated cells. Although cells from ID mice and those from mice repleted for 3 d incorporated slightly more radioactivity in cellular phospholipids than did cells from C or PF mice, less (P < 0.005) was recovered as IP than in controls, suggesting impaired conversion of the precursor to PIP2. At almost all incubation periods (10-120 min) and mitogen concentrations, the rate of PIP2 hydrolysis expressed as the ratio of radioactivity obtained in Con A-treated to untreated cells was significantly (P < 0.05) reduced in cells from ID mice compared with those obtained from C and PF mice. For cells that were activated for 60 min or less, iron repletion for 14 d significantly (P < 0.05) improved the rate of PIP2 hydrolysis. PIP2 hydrolysis positively and significantly (P < 0.05) correlated (r = 0.27-0.56) with indicators of iron status. Mitogenic response was also significantly (P < 0.05) reduced in ID but not PF mice, and it was corrected by iron repletion for 3, 7 or 14 d. Lymphocyte proliferation positively (r = 0.27-0.37, P < 0.01) correlated with indices of iron status and IP ratios. The data suggest that reduced PIP2 hydrolysis contributes to impaired blastogenesis in iron deficiency.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.