遗传肥胖易感性与出生后早期脂肪和瘦体重的关系：个体参与者荟萃分析。

Associations between genetic obesity susceptibility and early postnatal fat and lean mass: an individual participant meta-analysis.

机构信息

Medical Research Council Epidemiology Unit, University of Cambridge, Addenbrooke's Hospital, Cambridge, England.

Institut National de la Santé et de la Recherche Médicale, Center for Research in Epidemiology and Population Health, Lifelong Epidemiology of Obesity, Diabetes and Renal Disease Team, Villejuif, France3Medical Faculty, University Paris-Sud, Villejuif, Fr.

出版信息

JAMA Pediatr. 2014 Dec;168(12):1122-30. doi: 10.1001/jamapediatrics.2014.1619.

DOI:10.1001/jamapediatrics.2014.1619

PMID:25329327

Abstract

IMPORTANCE

Patterns of body size and body composition associated with genetic obesity susceptibility inform the mechanisms that increase obesity risk.

OBJECTIVE

To test associations between genetic obesity susceptibility, represented by a combined obesity risk-allele score, and body size or body composition at birth to age 5 years.

DESIGN, SETTING, AND PARTICIPANTS: A total of 3031 children from 4 birth cohort studies in England, France, and Spain were included in a meta-analysis.

EXPOSURES

A combined obesity risk-allele score was calculated from genotypes at 16 variants identified by genome-wide association studies of adult body mass index (BMI).

MAIN OUTCOMES AND MEASURES

Outcomes were age- and sex-adjusted SD scores (SDS) for weight, length/height, BMI, fat mass, lean mass, and percentage of body fat at birth as well as at ages 1, 2 to 3, and 4 to 5 years.

RESULTS

The obesity risk-allele score was not associated with infant size at birth; at age 1 year it was positively associated with weight (β [SE], 0.020 [0.008] SDS per allele; P = .009) and length (β [SE], 0.020 [0.008] SDS per allele; P = .01), but not with BMI (β [SE], 0.013 [0.008] SDS per allele; P = .11). At age 2 to 3 years these associations were stronger (weight: β [SE], 0.033 [0.008] SDS per allele; P < .001; height: β [SE], 0.025 [0.008] SDS per allele; P < .001) and were also seen for BMI (β [SE], 0.024 [0.008] SDS per allele; P = .003). The obesity risk-allele score was positively associated with both postnatal fat mass (1 year: β [SE], 0.032 [0.017] SDS per allele; P = .05; 2-3 years: β [SE], 0.049 [0.018] SDS per allele; P = .006; and 4-5 years: β [SE], 0.028 [0.011] SDS per allele; P = .009) and postnatal lean mass (1 year: β [SE], 0.038 [0.014] SDS per allele; P = .008; 2-3 years: β [SE], 0.064 [0.017] SDS per allele; P < .001; and 4-5 years: β [SE], 0.047 [0.011] SDS per allele; P < .001), but not with the percentage of body fat (P > .15 at all ages).

CONCLUSIONS AND RELEVANCE

Genetic obesity susceptibility appears to promote a normally partitioned increase in early postnatal, but not prenatal, growth. These findings suggest that symmetrical rapid growth may identify infants with high life-long susceptibility for obesity.

摘要

重要性

与遗传肥胖易感性相关的体型和身体成分模式为增加肥胖风险的机制提供了信息。

目的

检测遗传肥胖易感性（由肥胖风险等位基因评分代表）与出生至 5 岁时的体型或身体成分之间的关联。

设计、地点和参与者：在英格兰、法国和西班牙的 4 项出生队列研究中，共有 3031 名儿童参与了一项荟萃分析。

暴露情况

通过全基因组关联研究成人 BMI 确定的 16 个变体的基因型计算出肥胖风险等位基因评分。

主要结果和措施

结局是出生时以及 1、2 至 3 和 4 至 5 岁时体重、身长/身高、BMI、体脂肪量、去脂体重和体脂肪百分比的年龄和性别调整标准差评分（SDS）。

结果

肥胖风险等位基因评分与婴儿出生时的体型无关；在 1 岁时，它与体重（β[SE]，每等位基因 0.020[0.008]SDS；P=0.009）和身长（β[SE]，每等位基因 0.020[0.008]SDS；P=0.01）呈正相关，但与 BMI（β[SE]，每等位基因 0.013[0.008]SDS；P=0.11）无关。在 2 至 3 岁时，这些关联更强（体重：β[SE]，每等位基因 0.033[0.008]SDS；P<0.001；身高：β[SE]，每等位基因 0.025[0.008]SDS；P<0.001），并且 BMI 也呈正相关（β[SE]，每等位基因 0.024[0.008]SDS；P=0.003）。肥胖风险等位基因评分与出生后体脂肪量呈正相关（1 岁：β[SE]，每等位基因 0.032[0.017]SDS；P=0.05；2-3 岁：β[SE]，每等位基因 0.049[0.018]SDS；P=0.006；4-5 岁：β[SE]，每等位基因 0.028[0.011]SDS；P=0.009）和出生后去脂体重呈正相关（1 岁：β[SE]，每等位基因 0.038[0.014]SDS；P=0.008；2-3 岁：β[SE]，每等位基因 0.064[0.017]SDS；P<0.001；4-5 岁：β[SE]，每等位基因 0.047[0.011]SDS；P<0.001），但与体脂肪百分比无关（所有年龄的 P>0.15）。