FTO effect on energy demand versus food intake

John R. Speakman ()
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John R. Speakman: Institute of Biological and Environmental Sciences, University of Aberdeen

Nature, 2010, vol. 464, issue 7289, E1-E1

Abstract: Abstract Arising from: J. Fischer et al. Nature 458, 894–898 (2009)10.1038/nature07848 ; Fischer et al. reply An intronic single nucleotide polymorphism (SNP) (rs9939609) close to the fat mass and obesity associated gene (FTO) was the first SNP to be discovered with common variants linked to body mass index1; at least seven studies in humans have implicated this SNP with variations in food intake and satiety2,3,4,5,6,7,8, and four studies have rejected an effect on energy expenditure normalized for body weight2,5,6,8. Fischer et al.9 recently constructed a mouse in which the homologous Fto gene was inactivated (Fto-/-) and showed that these mice were protected from obesity. This observation strongly implicates the effects of the intronic SNP rs9939609 as arising due to an effect on the closest gene (FTO). However, the suggested mechanism underlying this effect in mice was opposite to that in humans. The Fto-/- mice showed no significant differences in food intake relative to wild-types litter-mates9 but had an elevated metabolic rate. The apparent contrasting effects of the gene in humans and mice is worthy of closer investigation.

Date: 2010
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DOI: 10.1038/nature08807

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