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The Gregg Lab has projects aimed at understanding the molecular links between nutrient stresses during critical early life periods and the lifetime risk for metabolic disease.
The goal of the work in the Gregg Lab is to characterize early life events that predispose individuals to developing type 2 diabetes and metabolic disease, with the ultimate goals of identifying interventions to improve insulin sensitivity, adiposity and type 2 diabetes risk in these individuals.
My interest in the critical window of infancy stems from research I conducted during my fellowship. This study used human pathology specimens to examine islet cell population dynamics across the lifespan. One of the goals of the project was to better define a critical window of beta-cell mass development so that future studies on early life events leading to a risk of type 2 diabetes would have a specified timeframe. This study highlighted the importance of the first 2 years of life for accrual of beta-cell mass and beta-cell proliferation.
The focus of the current research in the Gregg Lab is on understanding early life and developmental influences on pancreatic beta-cell function and determining factors that contribute to programming of type 2 diabetes risk.
We study the influence of perinatal exposure to anti-diabetic medications that impact cellular energy status and intracellular nutrient sensors, like metformin.
Another major focus of the lab is to understand the long-term metabolic programming effects of lactational nutrient exposures. We are taking a two-pronged approach: 1. examining milk composition in a human mother-infant cohort and 2. generating animal models of lactational programming.
Given the importance of early life for pancreatic beta-cell expansion, we also study the impact of nutrient stressors during the lactation period on postnatal pancreatic remodeling and islet function.
In future collaborative work we will also examine the impact of maternal metabolic disease on lactation physiology.
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