According to research published in the journal Nature, mutation in a protein that functions as a dietary fat sensor may cause obesity and liver disease.

A research team led by Professor Philippe Froguel, from the School of Public Health at Imperial College London, found that the protein GPR120, present on the cell surface in the gut, liver and fat tissue, if defected can raises the risk of obesity when fatty meals are eaten.

The new animal study highlights a target for new obesity treatment drug, as study authors found that mice that are deficient in GPR120 were 15% more prone to obesity and liver disease when placed on a high-fat diet. Scientists also found that the mice with deactivated GPR120 gene exhibited symptoms of fatty liver and diabetes.

Study authors compared the GPR120 gene of around 6,900 obese Europeans, who have fatty meals on a regular basis and found that Europeans with a mutation in the gene GPR120, which stops the protein from responding to omega-3 fatty acids, were significantly more likely to be obese, compared to those with no mutation.

Dr. Gozoh Tsujimoto, a professor at Kyoto University's department of genomic drug discovery science in Japan and study co-author advised doctors to recommend low-fat diet to people with the trait, adding that medications to reverse the effect of genetic trait can be developed.

Commenting on the discovery, Ruth Loos, director of Genetics of Obesity and Related Metabolic Traits at Mount Sinai School of Medicine in New York City, said the findings can help describe the causes of obesity, in turn aiding the development of weight loss treatment drug.

Read the original article here.