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 demands of the placenta and increased blood volume requirements) ID may threaten 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 may be associated with 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 are 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 which may alter it's developmental trajectory and therefore structure. In the proposed studies, the goal is to further identify the long-term effects of prenatal ID in adulthood, as our previous experiments have only characterized these effects at birth. Hence, using a model of iron deficiency in pregnancy, we will study 6-month old offspring to better understand how this common nutritional deficiency affects development and function of the kidney. Furthermore, we will assess how the kidney adapts to a common stressor, a high salt diet. The overall goal is to translate our findings and develop new therapeutic strategies to prevent the developmental abnormalities caused by ID in pregnancy.