Suppr超能文献

芬兰学龄儿童中肥胖遗传易感性与食物摄入对 BMI 的相互作用。

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

机构信息

Folkhälsan Research Center, Topeliuksenkatu 20, 00250, Helsinki, Finland.

Faculty of Medicine, University of Helsinki, Helsinki, Finland.

出版信息

Sci Rep. 2023 Sep 14;13(1):15265. doi: 10.1038/s41598-023-42430-5.

Abstract

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.

摘要

饮食可以调节肥胖的遗传风险,但很少有研究使用遗传风险评分(GRS)来研究儿童的这种调节作用。我们的目的是确定驱动特定食物与肥胖相互作用的单核苷酸多态性(SNP),并将这些 SNP 组合成 GRS。我们利用了芬兰青少年健康研究中的遗传和食物频率数据。共有 1142 名 11 岁的受试者在代谢芯片上进行了基因分型。计算了包含 30 个已知 SNP 的 BMI-GRS,并研究了个体 SNP 与食物及其综合饮食评分与年龄和性别特异性 BMIz 分数的相互作用。整个 BMI-GRS 与多种食物的 BMIz 相互作用。我们确定了每个相互作用的 7-11 个 SNP,并将这些 SNP 组合成特定食物的 GRS。最主要的相互作用发生在披萨(p<0.001):低风险人群的 BMIz 效应为 b-0.130(95%CI-0.23;-0.031),高风险人群的 BMIz 效应为 0.153(95%CI0.072;0.234)。相应地,我们还验证了甜食和巧克力、含糖果汁饮料、汉堡和热狗之间较弱的相互作用。这些相互作用共有 5 个 SNP,它们靠近 NEGR1、SEC16B、TMEM18、GNPDA2 和 FTO 基因。我们的研究结果表明,遗传上易患肥胖的儿童与 BMIz 之间的不健康食物的相关性比遗传易感性较低的儿童更强。这些相互作用的共享 SNP 表明代谢基因-饮食相互作用的共同差异,这值得进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37c1/10502078/660bf556c138/41598_2023_42430_Fig1_HTML.jpg

相似文献

3
Genetic risk score predicts risk for overweight and obesity in Finnish preadolescents.
Clin Obes. 2019 Dec;9(6):e12342. doi: 10.1111/cob.12342. Epub 2019 Oct 9.
5
Study of eight GWAS-identified common variants for association with obesity-related indices in Chinese children at puberty.
Int J Obes (Lond). 2012 Apr;36(4):542-7. doi: 10.1038/ijo.2011.218. Epub 2011 Nov 15.
6
Evaluating the interaction of common FTO genetic variants, added sugar, and trans-fatty acid intakes in altering obesity phenotypes.
Nutr Metab Cardiovasc Dis. 2019 May;29(5):474-480. doi: 10.1016/j.numecd.2019.01.005. Epub 2019 Feb 1.
7
Effects of Gene-Environment Interaction on Obesity among Chinese Adults Born in the Early 1960s.
Genes (Basel). 2021 Feb 13;12(2):270. doi: 10.3390/genes12020270.
8
BMI loci and longitudinal BMI from adolescence to young adulthood in an ethnically diverse cohort.
Int J Obes (Lond). 2017 May;41(5):759-768. doi: 10.1038/ijo.2016.233. Epub 2016 Dec 27.
10

引用本文的文献

1
Identification of SEC16B as a novel regulator of glucose homeostasis.
Diabetologia. 2025 Jul 24. doi: 10.1007/s00125-025-06501-8.
2
Young-onset type 2 diabetes-Epidemiology, pathophysiology, and management.
J Diabetes Investig. 2025 Jul;16(7):1157-1172. doi: 10.1111/jdi.70081. Epub 2025 May 24.
3
4
Variability of polygenic prediction for body mass index in Africa.
Genome Med. 2024 May 30;16(1):74. doi: 10.1186/s13073-024-01348-x.

本文引用的文献

1
Genomics and phenomics of body mass index reveals a complex disease network.
Nat Commun. 2022 Dec 29;13(1):7973. doi: 10.1038/s41467-022-35553-2.
2
The role of FTO variant rs1421085 in the relationship with obesity: a systematic review and meta-analysis.
Eat Weight Disord. 2022 Dec;27(8):3053-3062. doi: 10.1007/s40519-022-01509-0. Epub 2022 Nov 25.
3
Development of a genetic risk score for obesity predisposition evaluation.
Mol Genet Genomics. 2022 Nov;297(6):1495-1503. doi: 10.1007/s00438-022-01923-0. Epub 2022 Aug 10.
4
Central obesity in school-aged children increases the likelihood of developing paediatric autoimmune diseases.
Pediatr Obes. 2022 Mar;17(3):e12857. doi: 10.1111/ijpo.12857. Epub 2021 Oct 4.
6
Healthful plant-based dietary patterns, genetic risk of obesity, and cardiovascular risk in the UK biobank study.
Clin Nutr. 2021 Jul;40(7):4694-4701. doi: 10.1016/j.clnu.2021.06.018. Epub 2021 Jun 24.
9
10
Genetic risk score predicts risk for overweight and obesity in Finnish preadolescents.
Clin Obes. 2019 Dec;9(6):e12342. doi: 10.1111/cob.12342. Epub 2019 Oct 9.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验