New study evidence suggests that genetic variants can also be responsible for obesity.

Except eating disorder and poor lifestyle, sometimes a special gene variation can also make a person obese. A new research finding shows that the fat mass and obesity related protein gene, which is otherwise known as FTO, has direct contribution to abnormal weight gain. Although researchers were not unknown to the fact that FTO can have some sort of evil impact on a person’s body weight, this time they’ve made an extended effort to find out how exactly the alteration in the FTO can cause obesity.

It was an animal research. The study result is published in the May 6 issue of the Cell Metabolism. The earlier experiments, which tried to see the weight change in the mice after knocking out FTO, showed FTO variants might not cause obesity to all human beings. This recent initiative was to find out what variation of the FTO actually alters the function of the primary cilium. Cilium molecules can change the functions of the receptors for leptin. Leptin is a hunger suppressing hormone. The new research conducted by the scientists of Columbia University Medical Center indicates that the chances of obesity can be altered through a change in the function of the cilium.

Various aspects relating to obesity are still answered. With the help of the research finding, scientists are expecting to resolve many unexplored mysteries of obesity. The findings can give them clues. The recent animal study focusing role of FTO in obesity has been able to find out the core mechanism of the important molecules. If these molecules can be controlled and altered, the problem of obesity can be controlled to a great extent.

The research initiative has helped to find out gene RPGRIP1L. This gene is the major precursor of the complication. When Dr. Stratigopoulos, an associate research scientist, tried to determine if RPGRIP1L can trigger obesity, he introduced two mice without one of the two RPGRIP1L genes. As a result, those mice had reduced function of RPGRIP1L. Mice that had one of the genes RPGRIP1L, had a higher food intake and also gained more weight. This showed those mice had a higher percentage of body fat than the control.

Another study later found out that mice, which didn’t have RPGRIP1L, had an impaired leptin function. In all, it was clear that the gene RPGRIP1L had much to do with the function of the major hormone that can control hunger.

Although lack of energy balance causes obesity most of the times, after this disclosure regarding the FTO variation, it’s now clear that genetic variations can also cause this condition. So, if some people have still been trying to find out why they couldn’t lose weight despite the diet and lifestyle modification as suggested by his/her nutritionist, this could be a possible answer to that. People might expect to get another striking news relating to genetic variation and obesity relation because researchers are trying to find out how the RPGRIP1L changes the functions of the Leptin receptor. Overall, this could lead to an overwhelming possibility.