Funding outcome

Iron deficiency (ID) is the most common nutritional deficiency worldwide, affecting about 2 billion people. Because pregnant women are most at risk (due to blood volume expansion and the demands of the growing fetus and placenta) ID may threaten the early and lifelong health of not only the mother but also newborns. Some risks associated with ID in the developing child include anemia, growth restriction, and abnormal kidney development, which may, in turn, be associated with an increased risk of chronic heart and kidney disease in later life. Unfortunately, iron supplementation during pregnancy is often not effective, and these adverse pregnancy outcomes occur all too often. How ID causes these abnormal growth effects in the developing fetus is largely unknown, which poses a significant health risk for a large proportion of the population. Our lab recently found that ID causes higher levels of oxidative stress, and affects the ability of the mitochondria (the powerhouse of the cell) to generate energy in some fetal organs, such as the kidney and heart which may alter its development and hence long-term function. In the proposed studies, the goal is to further identify potential causes of the oxidative stress observed. Using a model of iron deficiency in pregnancy, we will study the genes that protect the cells against oxidative stress to determine if these are dysfunctional due to iron deficiency. Additionally, by looking at differences between males and females, we may gain insights into the differences between male and female susceptibility to stressors such as ID. The overall goal is to translate our findings and develop new therapeutic strategies to prevent the developmental abnormalities caused by ID in pregnancy.