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The gene mutation associated with obesity—the FTO gene—does not appear to regulate how calories are burned calories, but may influence the amount and choice of food consumed, according to a UK report published in The New England Journal of Medicine.
FTO gene mutations have shown the strongest association with obesity to date, Dr. Colin N. A. Palmer at the University of Dundee, Scotland, and colleagues point out. Yet, the mechanisms by which FTO mutations promote obesity have been unclear.
In 2,726 Scottish children between 4 and 10 years of age, the researchers tested for the FTO mutation rs9939609. All of the children underwent height and weight measurements. In 97 subjects, the link between the FTO mutation and amount of body fat, calories burned and food consumed was explored.
In all of the children, the mutation was associated with increased weight and body mass index, a commonly used determinant of obesity, the authors report. Testing in the subgroup also showed an association with elevated fat mass, but not with lean mass.
As noted, the FTO gene mutation was unrelated to regulation of calories burned. By contrast, the mutation was independently linked to increased food consumption, although the weight of food ingested did not differ significantly between the children with and those without the mutation.
“Variation within the FTO locus appears to confer a risk of obesity” through increased calorie intake, suggesting that moderate and controlled calorie consumption might prevent the development of FTO-related obesity, Palmer’s team concludes.
“This finding and its implications are especially important” due to growing evidence that childhood obesity is a major predictor of cardiovascular-related disease and death in adulthood, hey add.
SOURCE: The New England Journal of Medicine, December 11, 2008.