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A boy cries as he recuperates after surgery during "Operation Smile" at a hospital in Manila's Makati financial district October 26, 2009. Operation Smile aim to provide free surgery for about a hundred children inflicted with cleft lips, cleft palates, and other facial deformities over a period of five days in Makati.  REUTERS/Cheryl Ravelo

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    Mouse study sheds light on obesity gene

    LONDON
    Sun Feb 22, 2009 1:06pm EST

    LONDON (Reuters) - German scientists said on Sunday they had shown how a gene long associated with obesity might make people fat, a finding that could lead to new drugs to help control weight.

    Health  |  Lifestyle

    Mice without the FTO gene did not become obese and had less fat tissue overall because they burned off more calories even though they moved less and ate more, according to the study published in the journal Nature.

    FTO has been long linked to obesity. Studies have shown people with two copies of the "obese" version of the gene on average weigh nearly 7 lbs (3 kg) more and are about 70 percent more likely to be obese than those with other versions.

    People and mice are similar genetically.

    "So, this work provides a crucial piece of evidence supporting the notion that the FTO gene itself is likely to be involved in the effects of common human genetic variants on body fat," Stephen O'Rahilly of the University of Cambridge, who was not involved in the study, said in a statement.

    "This finding will promote research into the development of drugs that modulate FTO activity."

    Obesity, which raises the risk of diseases such as type 2 diabetes and heart problems, has increasingly become a global problem with people exercising less and leading more sedentary lifestyles.

    The World Health Organization classifies about 400 million people around the world as obese, and the numbers are increasing.

    In their study, Ulrich Ruther and colleagues at the University of Dusseldorf in Germany took a group of mice and knocked out, or inactivated, the FTO gene to see if they could figure out why the gene might make animals, and people, fat.

    Animals lacking the gene were thin because they spontaneously burned off many calories, suggesting FTO plays a direct role in controlling metabolism, they reported.

    "The human FTO gene has previously been shown to be linked to human obesity, however, this research helps unlock the complex interplay between factors expressed in the brain that control both appetite and metabolism," said David Cameron-Smith, an obesity expert at Deakin University in Australia.

    "A cure, genetic or pharmaceutical, for human obesity is many years away, although any new knowledge on how the brain controls hunger and growth will help solve the complex disease."

    (Reporting by Michael Kahn, Editing by Maggie Fox)



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