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.
JAMA Pediatr. 2014 Dec;168(12):1122-30. doi: 10.1001/jamapediatrics.2014.1619.
Patterns of body size and body composition associated with genetic obesity susceptibility inform the mechanisms that increase obesity risk.
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.
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).
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.
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).
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.
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。
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。
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。
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）。
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）。
遗传肥胖易感性似乎促进了出生后早期、但不是产前的正常、快速增长。这些发现表明，对称的快速生长可能会识别出终生肥胖易感性高的婴儿。
