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Role of the FTO Gene in Obesity

The FTO (Fat Mass and Obesity) gene is a nuclear protein of alpha-ketoglutarate dependent dioxygenase. Other names for this gene are ALKBH9, BMIQ14 and GDFD. In humans it is located on chromosome 16. The studies in mice and humans indicate that the FTO gene plays a role in nervous and cardiovascular systems and has a strong association with body mass index, obesity risk, and type 2 diabetes.

Role of variants of FTO gene in obesity –

Certain variants of the FTO genes appear to be correlated with obesity in humans. But that doesn't mean that people with the FTO gene variation are destined for obesity,

According to a large new study of Europeans, the researchers at the University of Oxford in the UK found that half of white Europeans have one defective copy of the FTO gene, which carries a 30% increased risk of obesity. But around 16% hold two altered copies of FTO, which carries a 70% increased obesity risk. They suspect that a similar proportion of other populations also hold the defective copies of FTO. Of the participants in the study, about 25% were obese.

Only 35% of this white European population had two normal copies of the gene. This study is significant because it has yielded evidence for the first obesity related gene.

The researchers also point out that the gene pool hasn’t changed in 20 or 30 years. So, it can be concluded that there are other factors despite FTO gene, which contribute to the obesity epidemic witnessed in many countries.

How does it cause obesity? –

Many are in a quandary as to the issue whether people with the FTO gene simply burn calories less efficiently or they consume more food. The following studies show how the FTO gene causes obesity.

In a new study, the researchers -- who included Joanne Cecil, PhD, of Scotland's University of Dundee -- studied some 2,700 elementary school kids in Scotland. They measured the children's height, weight, and waist and hip circumferences. They also checked the kids' FTO genes, based on saliva samples the students provided. As expected, the heavier children were more likely to have the FTO gene variant. Their extra weight came from fat mass, not lean tissue. A subgroup of 76 of these students got their metabolism monitored for 10 days and ate special meals at school. The researchers weighed the food before and after the meals to know how much the kids had eaten.

The researchers observed that kids having the FTO variant didn’t have sluggish metabolism but they ate more food, especially high calorie food, showing that the FTO variant seems to be involved in consumption of calories, not how the body handles those calories.

Further, in another study, brain scans of carriers of FTO variant appear to have decreased brain activity in areas of the brain associated with impulse control. The carriers may also have a "hardwired" preference to find eating high-fat food more enjoyable. Ongoing research did find that these carriers were more likely to become obese as they got older.

Conclusion –

The FTO gene has become a new buzzword. Many consider it to be the main culprit for obesity. In fact, people carrying the FTO gene variant can still achieve normal weight and maintain it with the help of specific lifestyle changes.

In a new study, the British researchers report that having the so-called "obesity gene" doesn't affect people's ability to shed pounds through diet, exercise and weight-loss medications. A person's environment may play a bigger part in weight management than their DNA, though the FTO gene is associated with increased body weight.

Obesity is a growing global public health crisis as an estimate indicates that 2.1 billion adults worldwide are overweight or obese. Therefore, ongoing efforts to curb the epidemic of obesity should focus on helping people find ways to live healthier, such as improving eating habits and getting regular physical exercise.

References -

American Journal of Epidemiology. 2010 Sep 15; 172(6): 653–665. Published online 2010 Aug 11. doi: 10.1093/aje/kwq178

New England Journal of Medicine 2008; 359: 2558-66

Molecular Psychiatry. Published online May 27 2014

British Medical Journal 2016; 354 doi: http://dx.doi.org/10.1136/bmj.i4707 (Published 20 September 2016)

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