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SUNDAY, Feb. 19 (HealthDay News) -- A new animal study suggests that a genetic mutation could put certain people at higher risk for becoming obese if they eat high-fat diets.
At the moment, the practical uses of the research seem to be limited, but physicians could conceivably test people for the mutation and recommend that they avoid certain kinds of diets, said study co-author Dr. Gozoh Tsujimoto, a professor at Kyoto University's department of genomic drug discovery science in Japan. It may also be possible, Tsujimoto said, to eventually give people drugs to combat the effects of the mutation.
If that happens, there would be "a new avenue for personalized health care," Tsujimoto said.
Scientists have been busy studying genetic links to obesity that could make some people more prone to gain extra weight. Two-thirds of Americans are either overweight or obese, the U.S. Centers for Disease Control and Prevention estimates. Excess pounds contribute to a variety of diseases, including heart disease and cancer.
In the new study, researchers looked at the component of the body's internal communication system that plays a role in the regulation of appetite and the production of fat cells.
The investigators found that mice that didn't have the component were 10 percent fatter than other mice when all were fed a high-fat diet. Mice without the component also developed higher intolerance to glucose.
Research conducted in animals does not always translate into humans, and much more research is needed. However, the researchers found that Europeans with the genetic mutation, known as GPR120, were more likely to be obese.
According to Tsujimoto, more than 3 percent of Europeans have the trait. The next step for researchers is to study its prevalence in Japanese, Korean and Chinese people.
What can be done with the knowledge from the study?
Tsujimoto said physicians could advise people with the trait to avoid high-fat diets. A test is available to detect the trait and it costs about $200 in Japan, Tsujimoto said.
While medications could potentially be developed that would reverse the effects of the genetic trait, there are no such drugs now, Tsujimoto added.
Ruth Loos, director of Genetics of Obesity and Related Metabolic Traits at Mount Sinai School of Medicine in New York City, said "these findings provide another piece of what turns out to be the very large puzzle that describes the causes of obesity."
Consistent findings in mice and humans have put the trait "more firmly on the obesity map and provides a new starting point for more research into the function of this gene," said Loos.
"This is only the beginning of likely many years of research to disentangle the physiological mechanisms that lie behind the link between this gene and obesity risk," she said. "It is only when we understand the physiology and biology better that one can start thinking of developing a drug."
The study appears online Feb. 19 in the journal Nature.
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