<i>SDCCAG</i>8基因<i>rs</i>12145833多态性在儿童肥胖干预中的作用

伍亚辉; 肖伍才; 陈敬; 宋洁云; 单蕊; 张瀚; 刘峥

doi:10.16835/j.cnki.1000-9817.2023.07.009

SDCCAG8基因rs12145833多态性在儿童肥胖干预中的作用

doi: 10.16835/j.cnki.1000-9817.2023.07.009

伍亚辉¹,
肖伍才¹,
陈敬¹,
宋洁云²,
单蕊¹,
张瀚¹,
刘峥^1, ,

1.
北京大学公共卫生学院妇幼卫生学系，北京 100191
2.
北京大学儿童青少年卫生研究所

基金项目:

国家自然科学基金项目 81903343

中央高校基本科研业务费资助 BMU2021YJ030

详细信息

作者简介:
伍亚辉(2001-)，男，湖南邵阳人，在读本科

通讯作者:
刘峥，E-mail：liuzheng@bjmu.edu.cn

利益冲突声明 所有作者声明无利益冲突。
中图分类号: Q343.1 R723.14 R179
计量
- 文章访问数: 380
- HTML全文浏览量: 173
- PDF下载量: 22
- 被引次数: 0
出版历程
- 收稿日期: 2023-04-10
- 修回日期: 2023-05-22
- 网络出版日期: 2023-07-25
- 刊出日期: 2023-07-25

The effect of rs12145833 polymorphism of SDCCAG8 gene on intervention of childhood obesity

1.
Department of Maternal and Child Health, School of Public Health, Peking University, Beijing(100191), China

摘要

摘要: 目的研究SDCCAG8基因rs12145833多态性在儿童肥胖干预中的作用，为基于遗传背景制定儿童肥胖个性化干预措施提供科学依据。方法于2018年9月—2019年6月，在一项整群随机对照试验中，选取393名北京地区8~10岁儿童作为研究对象，将8所学校以1∶1比例随机分为干预组与对照组，采集唾液DNA样本，检测SDCCAG8基因rs12145833多样性。对干预组进行综合干预，对照组不采取干预，干预措施包括饮食改善、体育运动、学校与家庭支持等；基线调查及干预1学年结束时测量肥胖相关指标。采用多元线性回归与Logistic回归分析基因与干预对肥胖指标的交互作用。结果干预组中，TT基因型儿童相较于GT和GG基因型儿童在干预后的收缩压(β=4.56，95%CI=1.84~7.28，P < 0.01)与舒张压(β=2.59，95%CI=0.45~4.73，P < 0.05)升高得更少；对照组中，TT基因型儿童相较于GT和GG基因型儿童的收缩压升高得更多(β=-2.86，95%CI=-5.63~-0.83，P < 0.05)；SDCCAG8基因rs12145833多态性与干预对儿童收缩压、舒张压、体脂率存在交互作用(P值均 < 0.05)。结论 SDCCAG8基因rs12145833位点TT基因型儿童相比于GG和GT基因型儿童对肥胖干预更敏感，尤其在收缩压、舒张压和体脂率改善上效果较好，仍需在不同种族人群中研究SDCCAG8基因rs12145833多态性在儿童肥胖干预中的作用。
- 基因 /
- 肥胖症 /
- 干预性研究 /
- 儿童 /
- 回归分析
Abstract: Objective To study the role of rs12145833 polymorphism of SDCCAG8 gene in the intervention of childhood obesity, so as to provide scientific basis for formulating personalized intervention measures based on genetic background in children with obesity. Methods From September 2018 to June 2019, a total of 393 children aged 8-10 years in Beijing were enrolled in a cluster randomized controlled trial. Eight schools were randomly allocated into intervention group and control group at a ratio of 1∶1. Saliva DNA samples were collected to detect rs12145833 polymorphism of SDCCAG8 gene. The intervention group received a comprehensive intervention, while the control group received usual practice. Intervention measures included diet improvement, sports, school amd family sport. The obesity related indicators were measured at baseline and after the end of intervention 1 academic year. Multiple linear regression and Logistic regression were used to analyze the interaction between genes and intervention on obesity indicators. Results In the intervention group, children with TT genotype of rs12145833 of the SDCCAG8 gene had less increase in systolic(β=4.56, 95%CI=1.84-7.28, P < 0.01) and diastolic blood pressure(β=2.59, 95%CI=0.45-4.73, P < 0.05) than those with GT and GG genotypes. In the control group, the systolic blood pressure of children with TT genotype increased more than those with GT and GG genotype(β=-2.86, 95%CI=-5.63--0.83, P < 0.05). There was an interaction between rs12145833 polymorphism of SDCCAG8 gene and intervention on systolic blood pressure, diastolic blood pressure and body fat percentage in children(P < 0.05). Conclusion Children with TT genotype of rs12145833 in the SDCCAG8 gene are more sensitive to obesity intervention than those with GG and GT genotypes, especially in the improvement of systolic blood pressure, diastolic blood pressure and body fat percentage. Further trials to study the role of rs12145833 polymorphism of SDCCAG8 gene in the intervention of childhood obesity among different ethnic populations are needed.
- Genes /
- Obesity /
- Intervention studies /
- Child /
- Regression analysis
注释:

1) 利益冲突声明 所有作者声明无利益冲突。

HTML全文

表 1 两组研究对象基线一般情况比较(x±s)

Table 1. Baseline data of the study subjects between two groups(x±s)

组别	人数	年龄/岁	身高/cm	体重/kg	腰围/cm	收缩压/mmHg	舒张压/mmHg	BMI/(kg·m^-2)	BMI Z评分	腰臀比	体脂率/%
干预组	200	9.55±0.29	140.5±6.95	36.99±9.38	65.00±10.45	101.8±9.91	56.80±6.66	18.57±3.71	0.72±1.46	0.85±0.06	21.16±10.77
对照组	193	9.57±0.31	139.7±6.83	35.92±8.91	64.42±9.92	100.5±9.84	56.69±5.97	18.23±3.29	0.61±1.40	0.84±0.06	20.25±9.43
t值		-0.60	1.09	1.16	0.56	1.30	0.18	0.97	0.80	1.20	0.88
P值		0.55	0.28	0.25	0.57	0.19	0.86	0.33	0.43	0.23	0.38
注： 1 mmHg=0.133 kPa。

下载: 导出CSV

表 2 两组儿童干预后肥胖相关指标的变化

Table 2. Changes of obesity-related indicators in the two groups of children after intervention

组别	基因型	人数	Δ腰围/cm	Δ收缩压/mmHg	Δ舒张压/mmHg	ΔBMI/(kg·m^-2)	ΔBMI Z评分	Δ腰臀比	Δ体脂率/%
干预组	TT	169	-0.97±10.57	-1.08±9.59	1.61±6.46	0.10±3.72	0.26±1.47	0.01±0.06	1.21±10.81
	GG+GT	31	-1.40±9.62	-6.05±11.64	-1.68±7.71	-0.03±3.67	0.21±1.43	0.01±0.06	0.21±10.53
对照组	TT	162	-1.36±10.13	-1.67±9.86	0.73±6.03	-0.40±3.37	0.04±1.44	0.01±0.06	-0.20±9.54
	GG+GT	31	-1.41±8.78	0.74±9.83	1.05±5.75	-0.13±2.86	0.16±1.17	0.01±0.05	0.42±8.88
注：正值表示干预后指标降低，负值表示干预后指标升高。

下载: 导出CSV

参考文献(14)

[1]	DONG Y H, CHEN L, LIU J Y, et al. Epidemiology and prediction of overweight and obesity among children and adolescents aged 7-18 years in China from 1985 to 2019[J]. Chin J Prev Med, 2023, 57: 11-19.
[2]	YANG L L, XI B. Childhood obesity and early target organ damage[J]. Chin J Prev Med, 2019, 53(7): 731-736.
[3]	XI B. Prevention of adult cardiovascular disease should start from childhood[J]. Chin J Prev Med, 2019, 53(7): 657-660.
[4]	LINDBERG L, DANIELSSON P, PERSSON M, et al. Association of childhood obesity with risk of early all-cause and cause-specific mortality: a swedish prospective cohort study[J]. PLoS Med, 2020, 17(3): e1003078. doi: 10.1371/journal.pmed.1003078
[5]	ZLATOHLAVEK L, VRABLIK M, MOTYKOVA E, et al. FTO and MC4R gene variants determine BMI changes in children after intensive lifestyle intervention[J]. Clin Biochem, 2013, 46(4/5): 313-316.
[6]	HEITKAMP M, SIEGRIST M, MOLNOS S, et al. Obesity genes and weight loss during lifestyle intervention in children with obesity[J]. JAMA Pedia, 2021, 175(1): e205142. doi: 10.1001/jamapediatrics.2020.5142
[7]	WANG H J, ZHANG H, ZHANG S W, et al. Association of the common genetic variant upstream of INSIG2 gene with obesity related phenotypes in Chinese children and adolescents[J]. Biomed Environ Sci, 2008, 21(6): 528-536. doi: 10.1016/S0895-3988(09)60013-1
[8]	SCHERAG A, DINA C, HINNEY A, et al. Two new Loci for body-weight regulation identified in a joint analysis of genome-wide association studies for early-onset extreme obesity in French and German study groups[J]. PLoS Genet, 2010, 6(4): e1000916. doi: 10.1371/journal.pgen.1000916
[9]	LIU Z, GAO P, GAO A Y, et al. Effectiveness of a multifaceted intervention for prevention of obesity in primary school children in china: a cluster randomized clinical trial[J]. JAMA Pediat, 2022, 176(1): e214375. doi: 10.1001/jamapediatrics.2021.4375
[10]	LIU Z, WU Y, NIU W Y, et al. A school-based, multi-faceted health promotion programme to prevent obesity among children: protocol of a cluster-randomised controlled trial (the DECIDE-children study)[J]. BMJ Open, 2019, 9(11): e027902. doi: 10.1136/bmjopen-2018-027902
[11]	DE ONIS M, ONYANGO A W, BORGHI E, et al. Development of a WHO growth reference for school-aged children and adolescents[J]. Bull World Health Organ, 2007, 85(9): 660-667. doi: 10.2471/BLT.07.043497
[12]	MAREES A T, DE KLUIVER H, STRINGER S, et al. A tutorial on conducting genome-wide association studies: quality control and statistical analysis[J]. Inter J Meth Psych Res, 2018, 27(2): e1608.
[13]	SCHERAG A, KLEBER M, BOES T, et al. SDCCAG8 obesity alleles and reduced weight loss after a lifestyle intervention in overweight children and adolescents[J]. Obesity (Silver Spring, Md), 2012, 20(2): 466-470.
[14]	LEE M J, FRIED S K. Integration of hormonal and nutrient signals that regulate leptin synthesis and secretion[J]. Ame J Physiol Endocrinol Metab, 2009, 296(6): E1230-E1238.