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儿童饮食行为对肥胖遗传易感性的介导作用。

Mediation of genetic susceptibility to obesity through eating behaviours in children.

作者信息

Goulet Danick, Boivin Michel, Gravel Christopher A, Little Julian, Potter Beth K, Dubois Lise

机构信息

School of Epidemiology and Public Health, University of Ottawa, Ottawa, Ontario, Canada.

Université Laval, Quebec, Quebec, Canada.

出版信息

Pediatr Obes. 2025 Apr;20(4):e13180. doi: 10.1111/ijpo.13180. Epub 2024 Oct 10.

DOI:10.1111/ijpo.13180
PMID:39390328
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11936709/
Abstract

BACKGROUND/OBJECTIVES: Few studies have examined the putative mediating role of eating behaviours linking genetic susceptibility and body weight. The goal of this study was to investigate the extent to which two polygenic scores (PGSs) for body mass index (BMI), based on child and adult data, predicted BMI through over-eating and fussy eating across childhood.

SUBJECTS/METHODS: The study sample involved 692 participants from a birth cohort study. Height and weight were measured on six occasions between ages 6 and 13 years. Over-eating and fussy eating behaviours were assessed five times between ages 2 and 6 years. Longitudinal growth curve mediation analysis was used to estimate the contributions of the PGSs to BMI z-scores mediated by over-eating and fussy eating.

RESULTS

Both PGSs predicted BMI z-scores (PGS: β = 0.26, 95% CI: 0.19-0.33; PGS: β = 0.34, 95% CI: 0.27-0.41). Over-eating significantly mediated these associations, but this mediation decreased over time from 6 years (PGS: 18.0%, 95% CI: 3.1-32.9, p-value = 0.018; PGS: 14.2%, 95% CI: 2.8-25.5, p-value = 0.014) to 13 years (PGS: 11.4%, 95% CI: -0.4-23.1, p-value = 0.057; PGS: 6.2%, 95% CI: 0.4-12.0, p-value = 0.037). Fussy eating did not show any mediation.

CONCLUSIONS

Our results support the view that appetite is key to translating genetic susceptibility into changes in body weight.

摘要

背景/目的:很少有研究探讨饮食行为在连接遗传易感性和体重方面的假定中介作用。本研究的目的是调查基于儿童和成人数据的两个体重指数(BMI)多基因分数(PGS)通过儿童期的暴饮暴食和挑食来预测BMI的程度。

对象/方法:研究样本包括来自一项出生队列研究的692名参与者。在6至13岁之间对身高和体重进行了6次测量。在2至6岁之间对暴饮暴食和挑食行为进行了5次评估。采用纵向生长曲线中介分析来估计PGS对由暴饮暴食和挑食介导的BMI z分数的贡献。

结果

两个PGS均能预测BMI z分数(PGS:β = 0.26,95%置信区间:0.19 - 0.33;PGS:β = 0.34,95%置信区间:0.27 - 0.41)。暴饮暴食显著介导了这些关联,但这种中介作用随时间从6岁时(PGS:18.0%,95%置信区间:3.1 - 32.9,p值 = 0.018;PGS:14.2%,95%置信区间:2.8 - 25.5,p值 = 0.014)降至13岁时(PGS:11.4%,95%置信区间: - 0.4 - 23.1,p值 = 0.057;PGS:6.2%,95%置信区间:0.4 - 12.0,p值 = 0.037)。挑食未显示出任何中介作用。

结论

我们的结果支持这样一种观点,即食欲是将遗传易感性转化为体重变化的关键。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/035e/11936709/53a360df5be0/IJPO-20-e13180-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/035e/11936709/2cf158f5b0c8/IJPO-20-e13180-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/035e/11936709/7ba231ffff28/IJPO-20-e13180-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/035e/11936709/53a360df5be0/IJPO-20-e13180-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/035e/11936709/2cf158f5b0c8/IJPO-20-e13180-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/035e/11936709/7ba231ffff28/IJPO-20-e13180-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/035e/11936709/53a360df5be0/IJPO-20-e13180-g003.jpg

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