Dataset Information

FTO genetic variants, dietary intake and body mass index: insights from 177,330 individuals.

ABSTRACT: FTO is the strongest known genetic susceptibility locus for obesity. Experimental studies in animals suggest the potential roles of FTO in regulating food intake. The interactive relation among FTO variants, dietary intake and body mass index (BMI) is complex and results from previous often small-scale studies in humans are highly inconsistent. We performed large-scale analyses based on data from 177,330 adults (154 439 Whites, 5776 African Americans and 17 115 Asians) from 40 studies to examine: (i) the association between the FTO-rs9939609 variant (or a proxy single-nucleotide polymorphism) and total energy and macronutrient intake and (ii) the interaction between the FTO variant and dietary intake on BMI. The minor allele (A-allele) of the FTO-rs9939609 variant was associated with higher BMI in Whites (effect per allele = 0.34 [0.31, 0.37] kg/m(2), P = 1.9 × 10(-105)), and all participants (0.30 [0.30, 0.35] kg/m(2), P = 3.6 × 10(-107)). The BMI-increasing allele of the FTO variant showed a significant association with higher dietary protein intake (effect per allele = 0.08 [0.06, 0.10] %, P = 2.4 × 10(-16)), and relative weak associations with lower total energy intake (-6.4 [-10.1, -2.6] kcal/day, P = 0.001) and lower dietary carbohydrate intake (-0.07 [-0.11, -0.02] %, P = 0.004). The associations with protein (P = 7.5 × 10(-9)) and total energy (P = 0.002) were attenuated but remained significant after adjustment for BMI. We did not find significant interactions between the FTO variant and dietary intake of total energy, protein, carbohydrate or fat on BMI. Our findings suggest a positive association between the BMI-increasing allele of FTO variant and higher dietary protein intake and offer insight into potential link between FTO, dietary protein intake and adiposity.

SUBMITTER: Qi Q

PROVIDER: S-EPMC4271061 | biostudies-literature | 2014 Dec

REPOSITORIES: biostudies-literature

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FTO genetic variants, dietary intake and body mass index: insights from 177,330 individuals.

Qi Qibin Q Kilpeläinen Tuomas O TO Downer Mary K MK Tanaka Toshiko T Smith Caren E CE Sluijs Ivonne I Sonestedt Emily E Chu Audrey Y AY Renström Frida F Lin Xiaochen X Ängquist Lars H LH Huang Jinyan J Liu Zhonghua Z Li Yanping Y Asif Ali Muhammad M Xu Min M Ahluwalia Tarunveer Singh TS Boer Jolanda M A JM Chen Peng P Daimon Makoto M Eriksson Johan J Perola Markus M Friedlander Yechiel Y Gao Yu-Tang YT Heppe Denise H M DH Holloway John W JW Houston Denise K DK Kanoni Stavroula S Kim Yu-Mi YM Laaksonen Maarit A MA Jääskeläinen Tiina T Lee Nanette R NR Lehtimäki Terho T Lemaitre Rozenn N RN Lu Wei W Luben Robert N RN Manichaikul Ani A Männistö Satu S Marques-Vidal Pedro P Monda Keri L KL Ngwa Julius S JS Perusse Louis L van Rooij Frank J A FJ Xiang Yong-Bing YB Wen Wanqing W Wojczynski Mary K MK Zhu Jingwen J Borecki Ingrid B IB Bouchard Claude C Cai Qiuyin Q Cooper Cyrus C Dedoussis George V GV Deloukas Panos P Ferrucci Luigi L Forouhi Nita G NG Hansen Torben T Christiansen Lene L Hofman Albert A Johansson Ingegerd I Jørgensen Torben T Karasawa Shigeru S Khaw Kay-Tee KT Kim Mi-Kyung MK Kristiansson Kati K Li Huaixing H Lin Xu X Liu Yongmei Y Lohman Kurt K KK Long Jirong J Mikkilä Vera V Mozaffarian Dariush D North Kari K Pedersen Oluf O Raitakari Olli O Rissanen Harri H Tuomilehto Jaakko J van der Schouw Yvonne T YT Uitterlinden André G AG Zillikens M Carola MC Franco Oscar H OH Shyong Tai E E Ou Shu Xiao X Siscovick David S DS Toft Ulla U Verschuren W M Monique WM Vollenweider Peter P Wareham Nicholas J NJ Witteman Jacqueline C M JC Zheng Wei W Ridker Paul M PM Kang Jae H JH Liang Liming L Jensen Majken K MK Curhan Gary C GC Pasquale Louis R LR Hunter David J DJ Mohlke Karen L KL Uusitupa Matti M Cupples L Adrienne LA Rankinen Tuomo T Orho-Melander Marju M Wang Tao T Chasman Daniel I DI Franks Paul W PW Sørensen Thorkild I A TI Hu Frank B FB Loos Ruth J F RJ Nettleton Jennifer A JA Qi Lu L

Human molecular genetics 20140807 25

FTO is the strongest known genetic susceptibility locus for obesity. Experimental studies in animals suggest the potential roles of FTO in regulating food intake. The interactive relation among FTO variants, dietary intake and body mass index (BMI) is complex and results from previous often small-scale studies in humans are highly inconsistent. We performed large-scale analyses based on data from 177,330 adults (154 439 Whites, 5776 African Americans and 17 115 Asians) from 40 studies to examine ...[more]

PMID: 25104851

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Project description:BACKGROUND:The risk of obesity is determined by complex interactions between genetic and environmental factors. Little research to date has investigated the interaction between gene and food intake. The aim of the current study is to explore the potential effect of fat mass and obesity-associated protein gene (FTO) rs9939609 and rs9930506 single nucleotide polymorphism (SNP) on the pattern of food intake in the Emirati population. METHODS:Adult healthy Emirati subjects with Body mass index (BMI) of 16-40 kg/m2 were included in the study. Genotyping for FTO rs9939609(A>T) and rs9930506(A>G) was performed using DNA from saliva samples. Subjects were categorized according to the WHO classification by calculating the BMI to compare different classes. Dietary intake was assessed by a sixty-one-item FFQ that estimated food and beverage intakes over the past year. The daily energy, macronutrient, and micronutrient consumption were computed. RESULTS:We included 169 subjects in the final analysis (mean age 30.49± 9.1years, 57.4% females). The mean BMI of the study population was 26.19 kg/m2. Both SNPs were in Hardy Weinberg Equilibrium. The rs9939609 AA genotype was significantly associated with higher BMI (p = 0.004); the effect was significant in females (p = 0.028), but not in males (p = 0.184). Carbohydrate intake was significantly higher in AA subjects with a trend of lower fat intake compared to other genotypes. The odds ratio for the AA was 3.78 in the fourth quartile and 2.67 for the A/T in the second quartile of total carbohydrate intake, considering the first quartile as a reference (95% CI = 1.017-14.1 and 1.03-6.88, respectively). Fat intake was significantly lower in the FTO rs9930506 GG subjects. The presence of FTO rs9930506 GG genotype decreased the fat intake in subjects with FTO rs9939609 AA (p = 0.037). CONCLUSIONS:The results of this study highlight the interaction of the FTO risk alleles on the food intake in Emirati subjects. The FTO rs9939609 AA subjects had higher carbohydrate and lower fat intake. The latter was accentuated in presence of rs9930506 GG genotype.

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FTO genetic variants, dietary intake and body mass index: insights from 177,330 individuals.

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FTO genetic variants, dietary intake and body mass index: insights from 177,330 individuals.

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