Summer
2011

Research Feature

Eating a Lot—But Staying Skinny

The Wounds of war

People struggling with weight may have suspected their genes were sabotaging their best efforts. Now, Colleen Croniger, PhD, a School of Medicine assistant professor of nutrition and genetics and director in the school's Mouse Metabolic Phenotyping Center, is conducting a study to assess this very thing.

Croniger and her colleagues are comparing the responses of two biologic models to eating a McDonald's-style high-fat diet: a normal, wild-type model and a so-called "A/J" model. "These A/J guys are like those people we hate, who can eat whatever they want and not exercise, and still don't gain an ounce," says Croniger.

The A/J model has a higher basic metabolism, the scientist explains, while the other model's lower metabolism leads him to store fat. So the scientists are asking, "What's protecting one but not the other from gaining weight and developing disease?" Croniger's team has zeroed in on a handful of genes in a small chromosomal region that could play a role in obesity (as well as NASH—nonalcoholic steatohepatitis—an obesity-associated, potentially serious liver disease marked by fat in the organ). The goal: to create new therapies to control people's expression of obesity-related genes.