Overexpression of Fto leads to increased food intake and results in obesity
By Chris D. Church, L. Moir, Fiona Mcmurray, C. Girard, G. Banks, L. Teboul, S. Wells, J. Bruning, P. Nolan, Frances M. Ashcroft and 1 more. Nature Genetics, 2010
718 citations recorded by the source corpus.
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.
Subfields: Genetics, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/03ee612a55967d26b4b30615a2c6bff42cc86c12
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Citations in the corpus
- N6-methyl-adenosine (m6A) in RNA: An Old Modification with A Novel Epigenetic Function (2012, background): “Although FTO has been known for its critical function in human obesity and energy homeostasis, its physiological substrates as a demethylase have been obscure [55–58].”
- Obesity-associated variants within FTO form long-range functional connections with IRX3 (2014, background): “Three enhancers (rectangles 3–5) drive reporter expression in lungs (3, 5) and brain (4).”