Obesity Caused by Genetic Mutation, Study Says
A new study on animals has implied that a genetic mutation could put certain people at higher risk of obesity if they eat high-fat diets.
Currently the new study's findings are limited, but physicians will likely test people for the mutation and be able to suggest that they avoid certain diets, said study co-author Dr. Gozoh Tsujimoto.
Tsujimoto, a professor at Kyoto University's department of genomic drug science in Japan, added that in the future it may be possible for people to take drugs to combat the effects of the mutation.
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If prescriptions could prevent weight gain, it would be "a new avenue for personalized health care," said the professor.
Obesity plagues millions of people around the world, including two-thirds of Americans, according to estimates by the U.S. Centers for Disease Control and Prevention. Excess weight can lead to several serious health issues, including heart disease and cancer.
Researchers have long suspected that genetics cause some people to be more prone to weight gain. The new study allowed researchers to examine the components of the body's internal communication system which controls appetite and the production of fat cells.
Although the research was conducted on animals, the information could also apply to humans, but more research is required.
"Our study for the first time demonstrated the gene responsible for diet-induced obesity," said Tsujimoto.
According to the professor, the researchers discovered the genetic mutation known as GPR120 in Europeans who were prone to weight gain. More than three percent of Europeans have the trait, and Tsujimoto said the next step is to study its prevalence in Japanese, Korean, and Chinese people.
In the future, a test for the gene could become available at $200, and doctors could advice patients with the gene on what diets to avoid.
Also, medications could potentially be developed to prevent the affects of the genetic mutation.
The study was published Sunday, and appears online in the journal Nature.
