Mary Loeken is an Investigator in the Section on Islet Cell and Regenerative Biology at Joslin Diabetes Center and an Associate Professor in the Department of Medicine at Harvard Medical School. She received her BA in Biology from Gonzaga University in Spokane, WA and her PhD in Reproductive Endocrinology at the University of Maryland School of Medicine in Baltimore, MD. Following postdoctoral training in the Laboratory of Molecular Virology at the National Cancer Institute, she joined the Research Division of Joslin Diabetes Center in 1988.
Dr. Loeken's laboratory studies the molecular causes of diabetic embryopathy, a diabetic complication in which the embryos of mothers with pregestational diabetes develop congenital malformations. Her laboratory developed a mouse model of diabetic pregnancy with which they have studied how maternal hyperglycemia causes neural tube defects, one of the most common malformations that occur in human diabetic pregnancy. They have delineated several biochemical processes that are perturbed by excess glucose metabolism and prevent induction of genes that are required for neural tube closure, and have demonstrated how abnormal embryo gene expression leads to apoptosis, causing a neural tube defect. Recently, they have established new mouse embryonic stem cell lines under physiological glucose and oxygen conditions. These cell lines replicate the metabolic and molecular responses of the embryo to normal and excess glucose exposure in a dish. The ultimate goal of her research is to advance methods to prevent, detect, or treat congenital malformations induced by diabetic pregnancy.
Dr. Loeken’s lab developed a mouse model of diabetic pregnancy that they have used to delineate several biochemical and molecular processes by which maternal diabetes causes congenital malformations, especially neural tube defects and cardiac outflow tract defects. More recently, they have employed embryonic stem cells as an in vitro model to complement their in vivo studies. The lab established new murine embryonic stem cell lines from blastocysts of both wild type and mutant mouse strains under physiological glucose and oxygen conditions (which is call, “LG-ESC”). These lines make it possible to study how increased glucose metabolism adversely affects embryo physiology and development at the cellular level. Of note, all of the responses downstream of increased glucose exposure (e.g., high KM glucose transport, hypoxic and oxidative stress, AMPK activity, gene expression changes, and p53 derepression) that we have observed in embryos are recapitulated in our LG-ESC lines. The long term goals of this research is to understand the mechanisms responsible for diabetic embryopathy and to potentially derive preventative treatments.
University of Maryland Medical School
National Institutes of Health
Distinguished Alumni Merit Award, Gonzaga University (2006)
John Stowers Research Award, Diabetic Pregnancy Study Group (2008)
Outstanding Alumna of the Year Award in Natural and Mathematical Sciences, UMBC (2013)