Defects in a dietary fat sensor may be behind obesity of many people, according to researchers at Imperial College London. The same defect can also lead to liver disease. The fat sensor protein is called GPR120 and it is located on the surface of fat tissue, gut and liver. These sensors react to unsaturated fatty acids from the diet including the omega-3 fatty acids that are very beneficial for health.
The experiment was conducted on mice that were fed high-fat diet. It was found that the mice who were deficient in GPR120 were more prone to becoming obese. In humans, it was found that those who had a gene mutation that restricted this protein from responding to omega 3 fatty acids were at a much increased risk of becoming obese. This is because when unsaturated fatty acid reacts with GPR120, the effect is release of hormones for suppressing appetite and stimulation of pancreas for secreting insulin.
The fat cells that exist in your body are informed about the increase in level of fats in the body, so to say, by the GPR120. This causes them to divide and produce more fat cells for storage of such extra fat. In this way, the risk of having a fatty liver as well as undue expansion of arteries does not arise. This mechanism can be responsible for some of the health benefits that we receive from omega-3 fatty acids.
This led Professor Philippe Froguel, from the School of Public Health at Imperial College London to comment that being overweight is not always unhealthy, provided you produced enough body cells in the body to store the fat. Those who are not able to process the fat in this way end up depositing it around their internal organs, and this is very unhealthy.
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