Dr. Wesolowski is an Associate Professor in the Department of Pediatrics, Section of Neonatology at the University of Colorado School of Medicine. View her biosketch here.
My long-term goal is to understand how altered nutrient supply programs fetal metabolism and how these changes may persist after birth and increase susceptibility to adult metabolic disease. My primary research is aimed to understand the effects of intrauterine growth restriction (IUGR) using integrative approaches in physiology and metabolism combined with novel molecular techniques in cell biology, epigenetics, and metabolomics. Current studies in our research program are focused on understanding the mechanisms for the early activation of fetal hepatic glucose production and development of hepatic insulin resistance, specifically the role of reduced glucose versus oxygen supply to the fetus, both key features of placental insufficiency and resulting IUGR. This is important in understanding why IUGR offspring have increased susceptibility to diabetes across their lifespan. I am also involved in projects investigating the effects of maternal high fat diet and obesity on offspring metabolism, specifically the early development of non-alcoholic fatty liver disease (NAFLD) and immune cell reprogramming.
My research builds upon on my prior work during my postdoctoral fellowship at University of Colorado and complements my previous training experiences in molecular endocrinology and physiology of metabolism during my graduate work at Cornell University. Overall, I am uniquely trained in large animal physiology, metabolism, and nutrition and have expertise in molecular and cellular biology. I have received a series of training and research grants from NIH-NIDDK including an F32, K01, R03, and R01. In addition, I am the sponsor on a F32 award and Co-I on an R24 award.
Current Projects in the lab with cellular metabolism, molecular biology, metabolic flux, and in vivo fetal physiology include:
- Molecular mechanisms for early development of fetal hepatic insulin resistance on suppression of glucose production in fetuses with IUGR
- Coordination of carbon and energy substrates (metabolic flux) within the liver and from other fetal organs and the placenta to support early activation of hepatic glucose production in IUGR fetus
- Role of hypoxia versus hypoglycemia in the early activation of fetal hepatic glucose production
- Effect of intrauterine exposures on fetal hepatic immune cell programming and function
- Mechanisms for early development of steatosis and NAFLD risk following exposure to maternal obesity
- Intrauterine intervention strategies to prevent later life metabolic disease risk