Publikation

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

Wissenschaftlicher Artikel/Review - 07.08.2014

Bereiche
PubMed
DOI

Zitation
Hansen T, Mozaffarian D, North K, Pedersen O, Raitakari O, Rissanen H, Tuomilehto J, Van der Schouw Y, Uitterlinden A, Zillikens M, Franco O, Shyong Tai E, Mikkilä V, Long J, Lohman K, Christiansen L, Hofman A, Johansson I, Jørgensen T, Karasawa S, Khaw K, Kim M, Kristiansson K, Li H, Lin X, Liu Y, Ou Shu X, Siscovick D, Uusitupa M, Cupples L, Rankinen T, Orho-Melander M, Wang T, Chasman D, Franks P, Sørensen T, Hu F, Loos R, Nettleton J, Mohlke K, Hunter D, Pasquale L, Toft U, Verschuren W, Vollenweider P, Wareham N, Witteman J, Zheng W, Ridker P, Kang J, Liang L, Jensen M, Curhan G, Qi L, Forouhi N, Qi Q, Xu M, Ahluwalia T, Boer J, Chen P, Daimon M, Eriksson J, Perola M, Friedlander Y, Gao Y, Heppe D, Holloway J, Asif Ali M, Li Y, Liu Z, Kilpeläinen T, Downer M, Tanaka T, Smith C, Sluijs I, Sonestedt E, Chu A, Renström F, Lin X, Ängquist L, Huang J, Houston D, Kanoni S, van Rooij F, Xiang Y, Wen W, Wojczynski M, Zhu J, Borecki I, Bouchard C, Cai Q, Cooper C, Dedoussis G, Deloukas P, Pérusse L, Ngwa J, Monda K, Kim Y, Laaksonen M, Jääskeläinen T, Lee N, Lehtimäki T, Lemaitre R, Lu W, Luben R, Manichaikul A, Männistö S, Marques-Vidal P, Ferrucci L. FTO genetic variants, dietary intake and body mass index: insights from 177,330 individuals. Hum Mol Genet 2014; 23:6961-72.
Art
Wissenschaftlicher Artikel/Review (Englisch)
Zeitschrift
Hum Mol Genet 2014; 23
Veröffentlichungsdatum
07.08.2014
eISSN (Online)
1460-2083
Seiten
6961-72
Kurzbeschreibung/Zielsetzung

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.