The London based research has published its findings in the Journal Of Clinical Endocrinology & Metabolism.
While studying the impact of the FTO gene on the ability to burn calories, researchers found that those children that had the gene’s risky variant don’t have their appetite switched off even after their stomachs are full.
The FTO is a gene on human chromosome 16. It has certain variants that appear to be correlated with obesity in humans. This link is has shown evidence in the Caucasian populations.
Studies have been conducted earlier to compare the weights of adults with and without the high risk version of the FTO gene. It shows that those adults with two copies of the gene are close to 3 kg heavier, those with a single copy of the gene are 1.5 kg heavier than adults without the gene.
Tests were also conducted on children between age 8 and 11, in order to find out if children carrying this high risk variant had changes in their appetite. The study consisted of height, weight and waist measurements as well a questionnaire asking parents about the eating habits of their children.
The results of the study were that children carrying the higher risk version of the gene had a tendency to overeat as they were unable to understand their appetite and know when they are full.
The effect of the gene on appetite was the same regardless of age, sex, socio-economic background and body mass index
define.
Professor Wardle, leading the research feels that when the gene is considered in isolation its effect is relatively small. She states that it was likely that many genes
define contributed to obesity and appetite by making small contributions individually. They create a substantial effect when brought together.
She quoted, "It is not simply the case that people who carry the risky variant of this gene automatically become overweight, but they are more susceptible to overeating. This makes them significantly more vulnerable to the modern environment which confronts all of us with large portion sizes and limitless opportunities to eat."
Dr David Haslam, clinical director of the National Obesity Forum, finds the research very interesting. He says that the findings are like the fitting of the first two pieces of a thousand piece jigsaw puzzle.
He said, "It is a step in the right direction, but what we don't want to say is that we have got the gene for obesity, therefore we can cure it. That is not going to happen for many years to come."
The researchers, from University College London and the Institute of Psychiatry, King's College London, set out to learn more about the way the gene works.
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