Timme-Laragy to Investigate Effects of Environmental Toxicants on Pancreatic Development

Associate professor of environmental health sciences Alicia Timme-Laragy has received a two-year, $421,400 grant from the National Institute of Environmental Health Sciences (NIEHS) to study the effects of environmental toxicants on pancreatic development.

Alicia Timme-Laragy
Alicia Timme-Laragy

The new funding is a result of Timme-Laragy’s research conducted while a UMass Amherst Center for Research on Families (CRF) Family Research Scholar. The year-long interdisciplinary faculty seminar provides a carefully selected group of UMass Amherst faculty the opportunities for peer mentorship, and national expert consultation to prepare a large grant proposal in support of their research.

“My CRF cohort provided important feedback on my proposal drafts, and the multidisciplinary perspectives were instrumental in shaping the research question behind this project,” says Timme-Laragy.

“The Center for Research on Families is pleased to support former CRF Scholar Dr. Timme-Laragy in her novel research on the effects of early-life exposures and redox stress on the pancreas and its implications for metabolic diseases,” says Lorraine Cordeiro, the director of the CRF and associate professor of nutrition. “Her scholarship advances research on families, promotes the significance of environmental health sciences in public health, enhances the stellar research profile of the School of Public Health and Health Sciences, and contributes to interdisciplinary scholarship at UMass Amherst.”

A developmental toxicologist with expertise in how early life exposures to PFAS (per and polyfluoroalkylated substances) and other environmental contaminants affect health, Timme-Laragy will examine how environmental toxicants trigger oxidative stress reactions in embryonic development using the zebrafish as a model system. Oxidative stress – an imbalance between the production of free radicals and antioxidant defenses in the body – can create a state called redox stress that damages cellular development and has been shown to cause metabolic dysfunction.

However, surprisingly little is known about how embryos respond to redox stress, or the impact of chemical exposures on pancreas development. Congenital pancreas malformations in humans are estimated to occur in approximately ten percent of the population and are associated with obesity, pancreatitis, Type 1 and Type 2 diabetes mellitus. The causes of these malformations are not well understood, and cannot be fully explained by genetic factors alone, suggesting a strong external component.

“We have found that early life exposures to PFAS compounds and pro-oxidants result in a shortened exocrine pancreas,” notes Timme-Laragy, who will take a systems-level approach to investigate the potential cellular and molecular mechanisms of oxidative stress that lead to this pancreatic deformity. “This work will help us understand the mechanisms by which these early-life exposures and redox stress can damage the developing pancreas and predispose humans to metabolic diseases.”