Malfunctioning Protein Linked To Obesity And Liver Disease

Malfunctioning Protein Linked To Obesity And Liver Disease

The researchers of the Imperial London College have conducted a study according to which the cause of liver disease and obesity is represented by malfunctions of a certain protein that is functioning as a dietary fat sensor. Their demonstrations emphasize the possibility of finding new drugs that can be used for treating metabolic disorders and obesity.

The culprit protein, GPR120, is located on the surface of the cells in the liver, gut and fat tissues and gives the cells the ability to detect and respond to the unsaturated fatty acids , mainly the omega-3 fatty acid which are known to have a very good impact on health. The researchers discovered through this study that mice short on GPR120 protein were more likely to develop obesity and liver diseases while being fed with high-fat food.  Another important finding of the study had to do with the fact that people having a certain mutation in the gene encoding this protein, thus stopping the GPR120 response to the omega-3 fatty acids, were more prone to become obese.

Faulty Protein

When the unsaturated fatty acid combined with the GPR120 protein in the gut, the hormones are released in order to decrease  the appetite and to stimulate the pancreas to generate the insulin. When the fatty cells feel the raised levels of fat in the blood, with the help of the GPR120 protein, they multiply in order to create more cells responsible for storing all the fat, thus decreasing the risk of fatty liver and furring of the arteries. This mechanism might represent an important way of highlighting some of the healthy  effects of the omega-3 acids.

When the lab mice were put on a diet based on high fat aliments, those individuals lacking the GPR120 not only  they have become obese but they also developed fatty livers, deficient control of blood glucose and lower numbers of fat cells. The scientists concluded that mice deficient in GPR120 have problems with the storage of the excess fat in the fat tissue. In return, their bodies deposit the fat in areas known to cause health disorders, such as the liver, the muscles and the walls of the arteries. For the human beings this form of obesity is associated with heart disease and type 2 diabetes.

The present study brought together scientists from Great Britain, France and Japan having the Professor Philippe Froguel, from the School of Public Health at Imperial College London, as the leader.

The gene of the GPR120 protein was analyzed on 6942 obese people and 7654 controls in order to discover if the differences in the code carrying the instructions for creating the protein, are responsible for the human obesity. Their resolution was that one mutation rendering the protein disorder increases a human’s obesity up to 60%. The researchers consider that the mutation of this protein echoes the effect of an unhealthy diet which lacks the unsaturated omega-3 fat.