Who or what is to blame for America's obesity epidemic?
Poor eating habits, a lack of willpower and sedentary lifestyles have all been suggested as causes. But new research indicates that unhealthy behaviors may not fully account for the problem.
Deborah Muoio, an assistant professor of medicine at Duke's Sarah W. Stedman Nutrition and Metabolism Center, helped discover an enzyme that is more highly expressed in obese people.
The enzyme, SCD1, prevents the burning of fat and increases fat storage in muscle cells-supporting the argument that obesity has a genetic component.
Muoio's study adds credibility and support to the small existing body knowledge about the genetic mechanisms of weight gain. "Obesity is caused by a combination of excess nutrition-based on an individual's metabolism-and a person's genetic vulnerabilities," said Muoio, the study's lead author. "The manifestation of obesity can only occur through this interaction of environment and genetics."
The enzyme is one of the few fairly conclusive genetic links to obesity, but it is only one aspect of a complex condition, said Christopher Newgard, professor of pharmacology and cancer biology and director of the Stedman Nutrition Center.
Muoio's team, which included researchers from Louisiana State University, said that the SCD1 gene's heightened activity in the muscle cells of obese patients is likely caused by environmental factors related to a person's nutrition and behavior.
The researchers forced muscle cells from lean patients to overproduce the SCD1 enzyme-which is normally about three times more active in muscle cells of obese people-and the cells produced substantial amounts of fat.
"Typically muscle cells among lean people need to store energy as lipids and carbohydrates to have easy access to it," Muoio said. "In this case leg and stomach muscle cells from lean subjects-once forced to produce more of the enzyme-mimicked the fat storage observed in obese subjects previously."
The ability to induce irreversible fat storage in cells from lean patients suggests that for obese individuals, lifestyle changes may come too late to combat genetic alterations. Consequently, subsequent weight loss and healthier lifestyle choices may not be as effective once the enzyme's production has been triggered.
"It's the first study that implicated this type of barrier to weight loss," Muoio said, noting that these findings further confirm the idea that obesity, like diabetes and other conditions, is a permanent affliction.
The study may also help to explain why so many obese people struggle to lose weight and keep it off.
"I think that there are obese people who are particularly genetically susceptible to becoming obese," said Dr. Howard Eisenson, director of the Duke's Diet and Fitness Center. "Once someone has become overweight, in some cases the highest level of determination isn't enough to maintain [weight loss]."
Muoio stressed, however, that because obesity has many causes, options still remain for those trying to lose weight.
"Exercise is a good counter-attack to this program," she said.
In addition to conventional weight loss methods, Newgard noted that drugs are also being developed to treat obesity, including some that target the SCD1 enzyme.
"There is a growing, promising body of knowledge that will slowly alter approaches to the issue [of obesity]," Newgard said.
In the future, a person's individual genomics and metabolism will likely play a hand in his or her treatment, he said.
In the meantime, researchers will continue to seek new approaches to combat the obesity epidemic.
"I don't think there's a one-stop shop for fighting obesity," Newgard said. "It's a complex issue-one we're working to break down to its cores."
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