The FTO Gene and Measured Food Intake in 5‐ to 10‐Year‐Old Children Without Obesity

Abstract

Objective: Genetic variation in the first intron of FTO (e.g., single-nucleotide polymorphism [SNP] rs9939609) is strongly associated with adiposity. This effect is thought to be mediated (at least in part) via increasing caloric intake, although the precise molecular genetic mechanisms are not fully understood. Prior pediatric studies of FTO have included youth with overweight and obesity; however, they have not informed whether a genotypic effect on ingestive behavior is present prior to obesity onset. Therefore, this study investigated the association between FTO and caloric intake in children aged 5 to 10 years without obesity (adiposity ≤ 95th percentile). Methods: A total of 122 children were genotyped for rs9939609 and ate ad libitum from a laboratory lunch buffet following a standardized breakfast. Linear regressions, adjusting for body mass, were used to examine the association between FTO "dose" (number of copies of SNP rs9939609) and intake variables. Results: There was a significant association between FTO and total intake. Each risk allele predicted an additional 64 calories, accounting for 3% of the variance. There were no associations between FTO and macronutrient preference, energy density, or diet variety. Results were influenced by race. Conclusions: Results corroborate and extend prior work by showing a dose-dependent effect on food intake in children without obesity.

The Impact of FTO Genetic Variants on Obesity and Its Metabolic Consequences is Dependent on Daily Macronutrient Intake

“…Another strength of our study is that it is based on a relatively large population. It is also worth noting that it has been shown that FTO genetic variants may influence dietary factors [ 14 , 40 , 41 , 42 ] or dietary fat intake [ 36 , 43 , 44 ], while other studies did not confirm these associations [ 12 , 15 ]. In general, we did not observe any significant differences in macronutrient intake between studied genotypes, which can also be interpreted as a strength of our study, because we can exclude the possibility that our results might be affected by the impact of different macronutrient intake on gene expression and the activation of different metabolic pathways.…”

Polygenic risk score for obesity and the quality, quantity, and timing of workplace food purchases: A secondary analysis from the ChooseWell 365 randomized trial

“…However, it remains unknown if genetic risk for obesity directly influences food choice behaviors and dietary intake. Obesity-implicated genetic variants may influence eating behaviors and obesity through a range of biological mechanisms that determine taste preferences, satiety, and cognitive and physiological responses to food and food cues [11][12][13][14][15]. Therefore, genetic predisposition to food choice behaviors may be in the causal pathway between genetic risk and the development of obesity, and genetic variants with CNS and non-CNS functions may contribute differentially to food choice behaviors.…”

Differences in brain structure and function in children with the FTO obesity‐risk allele

“…As part of the parent study, the relationship between FTO rs9939609 and total calorie intake was examined across a subgroup of 122 children—documenting significant association between FTO “dose” (number of copies of SNP rs9939609, adjusting for body mass) and total intake, but not macronutrient preference, energy density or diet variety 2 . Participants were included in the parent study if they were between the ages of 5 and 10, generally healthy and less than 95th body fat percentile (recruitment procedure are detailed elsewhere 2 ). In the course of the parent study, data were published suggesting that SNP rs1421085 addressed certain ancestry limitations inherent to SNP rs9939609 17 .…”