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Results: A meta-analysis of 10 studies (comprising 6951 participants) that reported the results of additive genetic models showed that individuals with the FTO TA genotype and AA genotype (those with the obesity-predisposing A allele) had .18-kg (95% CI: −0.09-, .45-kg; P = 0.19; NS) and .44-kg (95% CI: 0.09-, .79-kg; P = 0.015) greater weig.


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OBJECTIVE—To examine the longitudinal association of fat mass-and obesity-associated (FTO) variant with obesity, circulating adipokine levels, and FTO expression in various materials from human and mouse. RESEARCH DESIGN AND METHODS—We genotyped rs9939609 in 2,287 men and 3,520 women from two prospective cohorts.Plasma adiponectin and leptin were measured in a subset of diabetic men (n.


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The rs1421085 T-to-C single-nucleotide polymorphism (SNP) of the human FTO gene interrupts a conserved motif for ARID5B repressor, resulting in adipocyte type shift from beige to white.Methods: We obtained abdominal subcutaneous adipose tissue from donors carrying FTO rs1421085 TT (risk-free) or CC (obesity-risk) genotypes, isolated and differentiated their preadipocytes into beige adipocytes.


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Background: Children with rs9939609 FTO variant alleles (homozygous = AA and heterozygous = AT) are predisposed to greater adiposity than are those with 2 wild-type alleles (TT). Objective: Because FTO is highly expressed in hypothalamic regions that are important for appetite, FTO genotype may affect energy balance by influencing eating behavior.


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have been noted in several ethnic groups [22-27], includ-ing our previous report that FTO rs9939609 TT genotype was associated with obesity and preference for a high-fat diet in adult individuals from Jakarta [28]. Expression of the FTO gene also afects various parts of the brain that regulate energy balance and appetite [3, 29, 30].


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The FTO variant was significantly associated with body mass index (means in GG, GT and TT carriers were 28.7, 28.2 and 27.8 kg/m (2), p<0.001) and basal metabolic rate (BMR) (means in GG, GT and TT were 1603, 1588 and 1576 kcal per day, respectively, p<0.008) but it was not associated with physical activity, total energy intake or with energy in.


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The purpose of this study was to assess the connection between FTO rs9939609 (A/T) polymorphism and food preference. The study included 77 participants, 36 of whom were obese and had a low-calorie intake, and 41 non-obese participants with a high-calorie intake. Using a food frequency questionnaire (FFQ), the researchers calculated sweet and fatty food propensity scores. Genomic DNA was.


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This gene is a nuclear protein of the AlkB related non-haem iron and 2-oxoglutarate-dependent oxygenase superfamily but the exact physiological function of this gene is not known. Other non-heme iron enzymes function to reverse alkylated DNA and RNA damage by oxidative demethylation.


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Despite no evidence of any epistasis, we then went on to perform genotype combination analysis for rs9939609 and rs1544410, which showed that the FTO "AA" and VDR "CC" genotype combination and the FTO "TT" and VDR "CT" combination gave the highest and lowest mean BMI respectively (AA:CC-TT:CT; p = 0.016). This supports the fact.


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Association of the following genotypes was seen in those with ≥5% weight loss: TT of FTO polymorphism; 35 (81.4%) [OR (95% CI) AT, 2.5 (0.6, 10.9); TT, 6.9 (1.6, 28.2); with reference to AA],.


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Fat mass and obesity-associated protein also known as alpha-ketoglutarate-dependent dioxygenase FTO is an enzyme that in humans is encoded by the FTO gene located on chromosome 16. As one homolog in the AlkB family proteins, it is the first mRNA demethylase that has been identified. [5]


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The FTO A/T polymorphism (rs9939609) has been strongly associated with body mass-related traits in nonathletic populations, but rarely with elite athletic performance. The aim of the study was to investigate the association between the A/T polymorphism and athlete status in elite swimmers.


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Second, SGA-naïve children with the FTO rs9939609 A allele had higher fasting plasma glucose concentrations than SGA-naïve children with the TT genotype. This association between FTO genotype and fasting plasma glucose was not seen in SGA-treated children, Third, as predicted, in a subset of the children, those with the FTO rs9939609 A allele.


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However, when participants were stratified into higher and lower FTO methylation groups, the AA genotype possesses a 2.04-fold increased obesity risk in comparison to TT genotype (95%CI, 1.07-3.89.


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Women carrying the risk allele (TA or AA) of the FTO -rs9939609 genetic variant had a 1.16 kg/m 2 higher BMI over the follow-up period than those carrying the wild-type genotype (TT), even when.


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The lower levels of HDL were observed in AT/AA genotypes compared to the TT wild type genotype of FTO rs9939609 polymorphism (P = 0.004). Adjustments of age, BMI, and physical activity did not change the results. However, the significant association between FTO genotype and the HDL level was disappeared after further adjustments for dietary intake.