Previous studies from the Gannon laboratory have shown that in utero exposure to a western style diet results in enhanced glucose stimulated insulin secretion as well as an elevation in the beta to alpha cell ratio in offspring. Maternal overnutrition during gestation has been linked to adverse metabolic outcomes in offspring. My work focuses on the impact that metformin, a commonly prescribed Type 2 Diabetes therapeutic, has on beta cell development and mitochondrial dynamics in offspring in a non-human primate model of maternal overnutrition. While the target of metformin is unknown, metformin crosses the placenta, subjecting the fetus to the same dose of the drug measured in maternal circulation. The long-term effects of intrauterine exposure to metformin on the offspring has not been elucidated in a clinically relevant model. These studies highlight the developmental origins of metabolic risk factors that may confer increased susceptibility to metabolic disease of the offspring in adulthood.
