Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Genome-wide association studies have identified SNPs within FTO, the human fat mass and obesity-associated gene, that are strongly associated with obesity. Individuals homozygous for the at-risk rs9939609 A allele weigh, on average, ~3 kg more than individuals with the low-risk T allele. Mice that lack FTO function and/or Fto expression display increased energy expenditure and a lean phenotype. We show here that ubiquitous overexpression of Fto leads to a dose-dependent increase in body and fat mass, irrespective of whether mice are fed a standard or a high-fat diet. Our results suggest that increased body mass results primarily from increased food intake. Mice with increased Fto expression on a high-fat diet develop glucose intolerance. This study provides the first direct evidence that increased Fto expression causes obesity in mice.

Original publication

DOI

10.1038/ng.713

Type

Journal article

Journal

Nat Genet

Publication Date

12/2010

Volume

42

Pages

1086 - 1092

Keywords

Adiposity, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Animals, Area Under Curve, Body Temperature, Circadian Rhythm, Dietary Fats, Energy Metabolism, Feeding Behavior, Female, Glucose, Glucose Tolerance Test, Homeostasis, Male, Mice, Mixed Function Oxygenases, Models, Animal, Motor Activity, Obesity, Oxo-Acid-Lyases