The Roghair lab investigates the developmental origins of adult cardiometabolic disease across a number of model systems. This work originated with the realization that an adverse perinatal environment increases the risk of adult hypertension and obesity.
As a neonatologist, Dr. Roghair is driven to help bring a brighter future to premature infants. Premature infants are at an increased risk of hypertension, diabetes and obesity, and the risks are greatest in those born at the earliest gestations. With survival rates exceeding 90% for infants born as early as 23 weeks gestation, we are addressing critical knowledge gaps including longitudinal growth and body composition analysis, evidence-based nutritional recommendations and strategies to improve long-term cardiometabolic health. Our proposals leverage key clinical data, critical basic science discoveries and a team of interdisciplinary professionals to investigate quality improvement strategies and innovative therapeutic applications that could transform neonatal management with a positive impact on long-term cardiometabolic health. The figure below shows the profound leptin deficiency that develops following preterm delivery with postnatal blood levels far below the reference levels obtained from umbilical cord blood at the same gestation.
Mouse models of natural growth restriction and diet-based perturbations of the perinatal environment are currently being studied as they relate to cardiovascular, behavioral and metabolic outcomes. The Figure below demonstrates a normalization of adult learning when neonatal growth restriction-related leptin deficiency is prevented with neonatal leptin supplementation.
A significant percentage of pregnant women receive antidepressants during pregnancy. Although short-term side effects are manageable, there is emerging evidence intrauterine SSRI exposure may program adult cardiovascular and behavioral outcomes. Utilizing complementary mouse models and epidemiological studies, we are defining the molecular underpinnings of this “post-SSRI syndrome”.
Our proximity to the cystic fibrosis research groups at the University of Iowa led to our observation that the most common cystic fibrosis-causing mutation (CFTR-deltaF508) significantly impacts vascular tone. We are now aggressively assessing the effect of CFTR on arterial function in a number of species, including mice, pigs and humans that carry a copy of the CFTR-deltaF508 mutation.