Funding outcome

Studies on the developmental origins of health and disease (DOHaD) have demonstrated that perinatal stressors can alter developmental trajectories, and increase susceptibility to chronic disease in later life. Iron deficiency (ID) is one such stressor, for which pregnant women are at high risk; in Canada, a shocking 23% of women develop anemia during pregnancy. We have shown that prenatal ID causes sex and organ-specific complications in the fetus, which include reduced oxygen . delivery, dysfunction of the mitochondria-the powerhouse of the cell, and a higher production of reactive oxygen species (molecules which can damage components of the cell). The developing heart requires large amounts of energy for growth and function, and therefore may be particularly vulnerable to reduced oxygen delivery and mitochondrial dysfunction caused by ID during development. The objective of this work is to study how the heart grows in the wake of ID during development, and whether any changes in function persist in newborns. To complete this work, we will use a well-characterized rodent model of ID in pregnancy, and study various proteins indicative of heart damage and development. The proposed studies will be important in identifying therapeutic targets for new treatments for use in pregnancy that reduce or prevent chronic disease susceptibility due to ID.