Effects of theFTOGene on Lifestyle Intervention Studies in Children

Abstract

The effects of FTO on body weight, body composition, and the risk of developing overweight and obesity in children, adolescents, and adults are analyzed in this review. Most trails have been conducted on the rs9939609 SNP of the FTO gene. The minor A-allele frequency ranged from 0.38 to 0.49 in different European populations. Briefly, it has been reported that overweight-obesity risk per A-allele ranged from 1.76 to 1.35, whereas z-score for BMI has a wider variation from 0.05 to 0.5 kg/m² in European children and adolescents. As for other adiposity indexes, a waist circumference increase from 0.60 to 0.95 cm per A-allele was found together with an increase in fat mass from 0.68 to 1.78 kg in European children and adoles-cents. In regard to food intake, AA carrier subjects were reported to have reduced satiety responsiveness scores and a higher total energy and fat intake. However, it is not clear whether energy expenditure did modify the role of the rs9939609 FTO gene variant in adiposity. Furthermore, few reports examined the influence of FTO gene variants using intervention studies. Overall, it seems that the A-allele (rs9939609 FTO) is associated with higher body weight gain. However, further studies into FTO gene variants in children and adults are needed.

Obesity and eating behaviour in children and adolescents: Contribution of common gene polymorphisms

“…A small number of studies conducted in children have measured energy intake either directly or indirectly using parental report and show that the FTO locus confers risk of obesity through increasing energy intake (Cecil et al, 2008;Rendo et al, 2009;Timpson et al, 2008;Wardle et al, 2008b), through reduced satiety responsiveness and a preference for energy dense foods (Cecil et al, 2008;Lee et al, 2010;Tanofsky-Kraff et al, 2009;Timpson et al, 2008), but not through energy expenditure (Hakanen et al, 2009), supporting the adult literature (Haupt et al, 2009;Speakman et al, 2008). In a preload paradigm study, food intake from a test meal was signifi cantly increased in young children (4-10 years) carrying the minor (A) allele for FTO rs9939609, independent of body weight, through greater ingestion of energy dense foods, compared with wildtypes (Cecil et al, 2008).…”

The effect of rs9939609 FTO gene polymorphism on weight loss after laparoscopic sleeve gastrectomy

“…FTO regulates nutrition and energy homeostasis through its action on the leptin-melanocortin pathway in the hypothalamus [8,9]. The FTO gene, consisting of nine exons, was located on chromosome 16q12.2 [10], that it encodes a 2-oxoglutarate-dependent nucleic acid demethylase and that it is located in the nucleus [11,12]. Polymorphisms in FTO gene have been determined as genetic risk factors for obesity [13].…”

“…Notably SNP rs9939609, located in intron 1, is associated with a 31 % increase in the risk of developing obesity [14]. FTO gene polymorphism rs9939609 may have a place in the control of nutrition and food choice, proposing a possible relation to a hyperphagia or a preference for energydense foods [10]. Individuals with AA genotype for a rs9939609 having a 1.7-fold increased risk of obesity compared with TT individuals [15].…”

The combined effect of MC4R and FTO risk alleles on childhood obesity in Greece

“…6,7 Recent studies reveal a strong correlation between the rs9939609 A allele of the FTO and childhood obesity. 8,9 In this SNP, located in the first intron, threonine (T) is substituted by alanine (A) (T->A), this leading to a possible protein dysfunction that ultimately results in increased body weight.…”