Interaction between genetic susceptibility to obesity and food intake on BMI in Finnish school-aged children

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作者
Heli Viljakainen
Jose V. Sorlí
Emma Dahlström
Nitin Agrawal
Olga Portolés
Dolores Corella
机构
[1] Folkhälsan Research Center,Faculty of Medicine
[2] University of Helsinki,Department of Preventive Medicine and Public Health
[3] University of Valencia,Research Program for Clinical and Molecular Metabolism, Faculty of Medicine
[4] CIBER Fisiopatología de la Obesidad y Nutrición,Department of Nephrology
[5] University of Helsinki,undefined
[6] University of Helsinki and Helsinki University Hospital,undefined
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Diet modulates the genetic risk of obesity, but the modulation has been rarely studied using genetic risk scores (GRSs) in children. Our objectives were to identify single nucleotide polymorphisms (SNPs) that drive the interaction of specific foods with obesity and combine these into GRSs. Genetic and food frequency data from Finnish Health in Teens study was utilized. In total, 1142 11-year-old subjects were genotyped on the Metabochip array. BMI-GRS with 30 well-known SNPs was computed and the interaction of individual SNPs with food items and their summary dietary scores were examined in relation to age- and sex-specific BMI z-score (BMIz). The whole BMI-GRS interacted with several foods on BMIz. We identified 7–11 SNPs responsible for each interaction and these were combined into food-specific GRS. The most predominant interaction was witnessed for pizza (p < 0.001): the effect on BMIz was b − 0.130 (95% CI − 0.23; − 0.031) in those with low-risk, and 0.153 (95% CI 0.072; 0.234) in high-risk. Corresponding, but weaker interactions were verified for sweets and chocolate, sugary juice drink, and hamburger and hotdog. In total 5 SNPs close to genes NEGR1, SEC16B, TMEM18, GNPDA2, and FTO were shared between these interactions. Our results suggested that children genetically prone to obesity showed a stronger association of unhealthy foods with BMIz than those with lower genetic susceptibility. Shared SNPs of the interactions suggest common differences in metabolic gene-diet interactions, which warrants further investigation.
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  • [1] Albuquerque D(2017)The contribution of genetics and environment to obesity Br. Med. Bull. 123 159-173
  • [2] Yengo L(2018)Meta-analysis of genome-wide association studies for height and body mass index in approximately 700000 individuals of European ancestry Hum. Mol. Genet. 27 3641-3649
  • [3] Speakman JR(2018)GWAS for BMI: A treasure trove of fundamental insights into the genetic basis of obesity Int. J. Obes. 42 1524-1531
  • [4] Huang J(2022)Genomics and phenomics of body mass index reveals a complex disease network Nat. Commun. 13 7973-236
  • [5] Goodarzi MO(2018)Genetics of obesity: What genetic association studies have taught us about the biology of obesity and its complications Lancet Diabetes Endocrinol. 6 223-894
  • [6] Frayling TM(2007)A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity Science 316 889-61
  • [7] Loos RJ(2014)The bigger picture of FTO: the first GWAS-identified obesity gene Nat. Rev. Endocrinol. 10 51-647
  • [8] Yeo GS(2019)Ultra-processed food intake and risk of cardiovascular disease: Prospective cohort study (NutriNet-Sante) BMJ 365 639-1439
  • [9] Srour B(2009)The potential association between fruit intake and body weight—A review Obes. Rev. 10 1431-684
  • [10] Alinia S(2014)Dietary factors associated with metabolic risk score in Finnish children aged 6–8 years: The PANIC study Eur. J. Nutr. 53 671-1440