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Abstract
Emerging function of fat mass and obesity-associated protein (fto).
Highlights
Analyses of genetically engineered mouse models, in which the function of Fat Mass and Obesity-Associated Protein (Fto) is either eliminated [6,7,8] or enhanced [9], support a role of Fto in energy metabolism but are inconsistent as to whether Fto modulates caloric intake, energy expenditure, or both
Homozygous mice carrying a loss-of-function missense mutation in the C-terminal domain of Fto (367F) show no signs of perinatal lethality or growth retardation; they are lean, exhibit normal food intake and, when normalized by body weight, show increased energy expenditure [6]. While these studies appear to point to a potential role of Fto in regulating energy expenditure rather than food intake, mice globally overexpressing Fto are obese, hyperphagic, and exhibit normal energy expenditure when corrected for body fat or lean tissue mass [9]
The authors recapitulate that germline loss of Fto leads to perinatal lethality, growth retardation, and a lower body weight that is accompanied by decreased body fat and lean tissue mass
Summary
Analyses of genetically engineered mouse models, in which the function of Fto is either eliminated [6,7,8] or enhanced [9], support a role of Fto in energy metabolism but are inconsistent as to whether Fto modulates caloric intake, energy expenditure, or both. In 2009, global lack of Fto was reported to result in a lean phenotype as a consequence of increased energy expenditure [7].
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