Placental mTOR Regulation of Pancreatic Endocrine Cells

Type 2 diabetes is the most common chronic disease, but the search for causes and preventative treatment has largely failed. Our grant seeks to understand the mechanism controlling in utero growth restriction (IUGR), as there is evidence that type 2 diabetes is linked to this phenomenon. Human and animal models show that IUGR is a risk factor for diabetes because it influences the growth, development, and physiology of pancreatic-insulin producing beta-cells. Dr. Alejandro will investigate the role of the nutrient-sensor mTOR in the placenta in regards to the development of beta-cells and other endocrine cells (Aim1) and how mTOR signaling influences nutrient availability to the embryo to promote pancreatic endocrine cell development or growth (Aim2). Therefore, the successful completion of this grant will define mechanisms of placental mTOR on endocrine cell development, which could lead to potential molecular targets for regenerative medicine and identifying individuals at risk for type 2 diabetes, thereby advancing clinical care.