Consequences of Maternal Iron‐Deficiency: Fetal Anemia, and Hypoxia in Select Tissues of the Conceptus

Iron deficiency (ID) is the most prevalent nutritional deficiency worldwide, and affects populations across the socio‐economic spectrum. The incidence of ID anemia in pregnant women is of chief concern, with rates as high as 80 % in developing countries, and a prevalence of 23 % in Canada. Maternal ID during pregnancy has been shown to impact fetal iron status and growth trajectories, although the precise mechanisms underlying this intrauterine growth restriction are unknown. We hypothesized that maternal ID causes fetal hypoxia, resulting in asymmetric growth restriction in more severe ID. Female rats (initial age 6 weeks for severe (S‐ID), 9 weeks for moderate (M‐ID)) were fed iron restricted diets throughout pregnancy. Dams were treated with pimonidazole on gestational day (GD)20 to assess hypoxia (<10 mm Hg O 2 ). Maternal and fetal hemoglobin (Hb) levels and body weights were assessed on GD21. Pup organs were excised and weighed to assess degree of asymmetric growth restriction. Tissue immunofluorescence was carried out on GD21 pup tissues with fluorescent probes to detect covalent pimonidazole adducts. Both M‐ and S‐ID groups caused fetal anemia ( fetal Hb reduced 30.9 % and 63.8 %, respectively, compared to control of 9.27 g/dL, P<0.01), despite only S‐ID dams becoming anemic (reduction in Hb 10.9 % and 50.3 % for M‐ and S‐ID, respectively, compared to 13.60 g/dL control Hb, P<0.001). Both M‐ and S‐ID caused fetal growth restriction (reduced weight by 9.1 % and 34.9 %, respectively, compared to control weight of 5.45 g, P<0.001). S‐ID, but not M‐ID, caused asymmetrical growth restriction, wherein relative heart and brain weights increased (60 % and 9.8 %, respectively, compared to control weights of 0.005 g/g and 0.041 g/g, P<0.01), and kidney and liver size decreased (20 % and 15 %, respectively, compared to control weights of 0.005 g/g and 0.067 g/g, P<0.01). M‐ID was associated with increased staining for pimonidazole in fetal livers (P=0.01) and kidneys (P=0.01), but not in brains and placentae, versus respective controls; hypoxia staining is S‐ID fetuses is ongoing. Fetal anemia and growth restriction can occur in the absence of maternal anemia, emphasizing the need for new methods of assessment in the clinical setting. Elucidation of the mechanisms through which ID impacts fetal growth and development will enable us to develop a platform with which we can test novel therapeutics. Support or Funding Information AW held an Alberta Innovates Health Solutions Summer Studentship. SB Holds grants from the Canadian Institute of Health Research (CIHR), and the Women and Children's Health Research Institute (WCHRI).

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