Hometown: Daytona Beach, FL
Education: BS from Duke University
Research Topic: Non-human primates and high-fat diets, gestational diabetes.
The Developmental Origins of Health and Disease Hypothesis postulates that the gestational environment influences postnatal health and plays a role in disease etiology. Data from animal models and humans has demonstrated that the in utero environment significantly influences the offspring's risk of developing metabolic disease like Type 2 Diabetes later in life. My work focuses on investigating the effects of in utero high fat diet exposure on pancreatic islet morphology and gene expression in 3 year old non human primates. The mechanism by which disease risk is increased in offspring exposed to high fat diet in utero is thought to be epigenetic. Thus, I will explore the extent to which maternal diet influences histone modifications in the beta cells of a mouse model of maternal overnutrition. These studies will help elucidate the mechanisms by which maternal diet influences the risk of diabetes in non human primates and mice.
During pregnancy, maternal β-cells undergo compensatory changes including increased β-cell mass, improved glucose sensitivity, and enhanced glucose-stimulated insulin secretion. Failure of these adaptations to occur results in gestational diabetes.
I am studying the role of Connective tissue growth factor (Ctgf) in glucose homeostasis and islet physiology during pregnancy. Female mice with conditional loss of Ctgf from the endocrine cells develop gestational diabetes due to impaired glucose-stimulated insulin secretion. Heterozgyosity for Ctgf also impairs pregnancy-induced β-cell proliferation, demonstrating that this protein has multiple roles in islet biology. The impact of Ctgf on both β-cell proliferation and function suggests that Ctgf could be used as a therapeutic to expand functional β-cell mass in humans.