URI_Research_Magazine_2010-2011_Melissa-McCarthy

multi- and interdisciplinary research

Maybe It’s not the Junk Food Making us Fat

With obesity on the rise – 60 percent of Americans are now considered overweight – and with it a number of weight-related medical problems such as heart disease and type 2 diabetes, the questions of how and why people get fat have assumed new urgency. In her laboratory at the University of Rhode Island (URI), Angela Slitt, assistant professor of biomedical and pharmaceutical science, is seeking answers to these questions. With a $2.1 million grant from the National Institute of Environmental Health Sciences, Slitt is looking at how drug transporters enable chemicals to permeate the body’s liver and kidneys and how reducing weight might affect these vital agents. Of particular concern to Slitt is the chemical bisphenol A (BPA), which is found in a number of hard plastic products, including baby bottles. Early exposure to BPA, either as an infant or in the womb, has been shown to affect fat cells, which in turn might explain why childhood obesity is now a national epidemic. In other words, it might not be the junk food. Genetics, junk food, and a sedentary lifestyle have not been discounted as reasons for obesity, but beginning about five years ago, BPA exposure has also been cited as a possible cause, opening the door to what many consider to be an exciting new line of scientific study.

“It’s a relatively new concern,” said Slitt. New, but definitely getting a lot of attention not only in the scientific community, but also in the popular press, where headlines such as “Born to be Big” and “Is Plastic Making Us Fat?” have topped recent articles in Newsweek magazine and the Boston Globe newspaper, among other mainstream publications. Studies with mice and rats have shown that when a pregnant mother is exposed to BPA, there’s an increased likelihood that her offspring will be obese, Slitt said. In addition, researchers know that the liver and kidneys of obese rodents look different from those of rodents with normal weight. For Slitt, the issue is drug transporters, which she likened to tiny pumps that sit on top of a cell’s membrane and regulate the flow of chemicals – in this case BPA – traveling in and out of the cell. The specific questions Slitt and her research team are trying to answer is what happens to drug transporters if people lose weight. Will they work the same as they did before to control exposure to chemicals such as BPA? Or does weight gain permanently alter this process? Once overweight, are obese people at greater risk of exposure to BPA and other chemicals, or can this process be reversed? “Our goal is to understand whether BPA disposition changes with obesity,” said Slitt. The purpose of her research is to find out whether the obese population has a “different body burden.”

The University of Rhode Island 18