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中华肥胖与代谢病电子杂志 ›› 2026, Vol. 12 ›› Issue (02) : 140 -148. doi: 10.3877/cma.j.issn.2095-9605.2026.02.009

循证医学

基因多态性与环境因素交互作用对儿童肥胖影响的Meta分析
张频1, 袁薇婷2, 杨红叶3,()   
  1. 1214400 江阴,江阴市妇幼保健院检验科
    2214400 江阴,江阴市妇幼保健院医教科
    3江阴市第三人民医院儿科
  • 收稿日期:2026-06-18 出版日期:2026-05-31
  • 通信作者: 杨红叶

Interplay between genetic polymorphisms and environmental factors in childhood obesity: a meta-analysis

Pin Zhang1, Weiting Yuan2, Hongye Yang3,()   

  1. 1Department of Clinical Laboratory, Jiangyin Maternal and Child Health Hospital, Jiangyin 214400, China
    2Department of Medical Education, Jiangyin Maternal and Child Health Hospital, Jiangyin 214400, China
    3Department of Pediatrics, Jiangyin Third People’s Hospital, Jiangyin 214400, China
  • Received:2026-06-18 Published:2026-05-31
  • Corresponding author: Hongye Yang
引用本文:

张频, 袁薇婷, 杨红叶. 基因多态性与环境因素交互作用对儿童肥胖影响的Meta分析[J/OL]. 中华肥胖与代谢病电子杂志, 2026, 12(02): 140-148.

Pin Zhang, Weiting Yuan, Hongye Yang. Interplay between genetic polymorphisms and environmental factors in childhood obesity: a meta-analysis[J/OL]. Chinese Journal of Obesity and Metabolic Diseases(Electronic Edition), 2026, 12(02): 140-148.

目的

对肥胖相关基因多态性以及可干预环境因素的交互作用,如何影响儿童超重和肥胖进行系统评估。

方法

检索按照PRISMA流程进行,时间范围是各库建库到2026年4月1日,把超重或肥胖儿童及青少年的研究纳入考察范围。连续型结局以标准化均数差(SMD)来表示,二分类结局则用比值比(OR)来表示,且都经过随机效应模型的合并。异质性用I2来衡量,发表偏倚靠漏斗图进行定性判断。

结果

共纳入23篇文献。FTO效应等位基因携带者与非携带者相比,合并SMD为-0.13(95%CI:-0.34~0.08,I2=39%),差异未达到统计学意义。MC4R与饮食的交互纳入9项研究,rs17782313 C等位基因携带者的合并OR为1.35(95%CI:1.19~1.53,I2=0%,P<0.0001),风险较非携带者约高35%,各研究方向一致、结果稳健。睡眠方面纳入8项研究,睡眠不足儿童超重/肥胖的合并OR为1.54(95%CI:1.26~1.87,I2=53%,P<0.0001);因研究间异质性处于中至高水平,此合并值需谨慎解读。

结论

儿童肥胖是由遗传易感因素和可调控环境因素共同作用引起的,遗传背景会增加环境暴露致胖的风险。

Objective

To investigate the relationship between genetic polymorphisms and environmental factors, we conducted a meta-analysis.

Methods

According to the PRISMA guidelines, we conducted a systematic search across all relevant databases from the inception of the search until April 1, 2026. We also retained studies that addressed the interaction between obesity-related gene polymorphisms and modifiable environmental factors in overweight or obese children and adolescents. Continuous outcomes were summarized as standardized mean differences (SMD) and dichotomous outcomes as odds ratios (OR), with effect sizes combined under a random-effects model; heterogeneity was assessed by I2 statistic, and publication bias was judged qualitatively from funnel plots.

Results

23 studies meet the criteria. For FTO effect-allele carriers versus non-carriers, the pooled SMD was -0.13 (95%CI: -0.34 to 0.08, I2= 39%), a difference that did not reach statistical significance. Nine studies addressed the MC4R-diet interaction: carriers of the rs17782313 C allele showed a pooled OR of 1.35 (95%CI: 1.19 to 1.53, I2=0%, P<0.0001), roughly a 35% higher risk than non-carriers, with effect directions consistent and the result robust across studies. Eight studies informed the sleep analysis, where insufficient sleep carried a pooled OR for overweight/obesity of 1.54 (95%CI: 1.26 to 1.87, I2= 53%, P<0.0001); given the moderate-to-high heterogeneity, this estimate should be read with caution.

Conclusion

Childhood obesity is a result of both genetic predisposition and modifiable environmental factors, with genetic factors contributing to the risk.

图1 研究文献筛选流程
表1 纳入研究的基本特征
纳入研究(第一作者,年份) 国家/地区 基因(位点) 交互因素 主要结局指标
Cecil 2008 英国 FTO rs9939609 饮食/能量摄入 能量摄入/BMI(SMD)
Wardle 2008 英国 FTO rs9939609 饮食/饱腹感 能量摄入/BMI(SMD)
Timpson 2008 英国 FTO rs9939609 饮食/能量摄入 能量摄入/BMI(SMD)
Hakanen 2009 芬兰 FTO rs9939609 饮食/能量摄入 能量摄入/BMI(SMD)
Liu 2010 美国 FTO rs9939609 饮食/能量摄入 能量摄入/BMI(SMD)
Lee 2010 韩国 FTO rs9939609 饮食/能量摄入 能量摄入/BMI(SMD)
Jääskeläinen 2013 芬兰 MC4R rs17782313 进食频率/饮食 超重/肥胖(OR)
Lauria 2016 欧洲 MC4R rs17782313 饮食 超重/肥胖(OR)
Mohsenipour 2022 伊朗 MC4R rs17782313 饮食 超重/肥胖(OR)
Muller 2014 美国 MC4R 饮食 超重/肥胖(OR)
Obregón 2017 智利 MC4R rs17782313 进食行为/食物奖赏 超重/肥胖(OR)
Stutzmann 2009 法国/欧洲 MC4R 进食行为 超重/肥胖(OR)
Valladares 2010 智利 MC4R 进食行为 儿童肥胖(OR)
Wang 2017 中国 MC4R rs12970134 食欲/饮料摄入 超重/肥胖(OR)
Yeum 2025 美国 MC4R 无饥饿进食/饮食 超重/肥胖(OR)
Chan 2014 美国 DRD2/ANKK1 睡眠问题 超重(OR)
Fu 2019 中国 多基因(瘦素通路) 睡眠时长 超重/肥胖(OR)
Jiang 2019 中国 FTO rs9939609 睡眠等生活方式 肥胖指标(OR)
Krishnan 2017 新西兰 CLOCK/PEMT/GHRELIN 睡眠时长 肥胖相关性状(OR)
Meng 2020 美国 CLOCK rs1801260 睡眠(性别修饰) BMI(OR)
Nascimento Ferreira 2018 欧洲 REV-ERBα 睡眠时长 BMI(OR)
Prats-Puig 2013 西班牙 FTO/TMEM18/NRXN3 短睡眠 体重增加易感(OR)
Zhu 2020 中国 CMTM7 rs347134 膳食模式 肥胖(OR)
图2 FTO基因与饮食的交互作用
图3 MC4R基因与饮食的交互作用
图4 睡眠时间不足或存在睡眠问题与超重风险
图5 偏倚风险与总结
图6 发表偏倚分析。A:FTO-饮食,B:MC4R-饮食,C:睡眠-超重
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