Hinney Anke, Wolters Barbara, Pütter Carolin, Grallert Harald, Illig Thomas, Hebebrand Johannes, Reinehr Thomas
J Pediatr Endocrinol Metab. 2013;26(11-12):1209-13. doi: 10.1515/jpem-2013-0179.
An obesity risk allele at the NEGR1 locus was shown to be associated with weight regain after a lifestyle intervention in obese adults. Independent confirmation and studies in children are lacking. Therefore, we analyzed the impact of this and 11 additional obesity susceptibility loci on weight regain after a lifestyle intervention in overweight children.
We longitudinally analyzed the changes in weight status as body mass index standard deviation score (BMI-SDS) in 282 overweight children (10.6 ± 2.5 years, 47% male, BMI 27.1 ± 3.9 kg/m2) both at the end of a 1-year lifestyle intervention and at 1 year after the end of intervention. We genotyped obesity risk single nucleotide polymorphisms (SNPs) derived from genome-wide association studies in or in proximity to the following genes: NEGR1, TNKS, SDCCAG8, FTO, MC4R, TMEM18, PTER, MTCH2, SH2B1, MAF, NPC1, and KCTD15.
The children reduced their BMI-SDS (-0.28 ± 0.35; p<0.001) during intervention and increased their BMI-SDS between the end of intervention and 1 year later (+0.05 ± 0.36; p=0.027). None of the SNPs including NEGR1 was related significantly to weight regain.
We found no evidence for effects of any of the GWAS-based obesity marker alleles on weight regain in the course of 1 year after an intervention.
在肥胖成年人中，NEGR1基因座的肥胖风险等位基因被证明与生活方式干预后的体重反弹有关。但缺乏独立验证以及在儿童中的研究。因此，我们分析了该基因座以及另外11个肥胖易感基因座对超重儿童生活方式干预后体重反弹的影响。
我们纵向分析了282名超重儿童（10.6±2.5岁，47%为男性，BMI 27.1±3.9kg/m²）在1年生活方式干预结束时以及干预结束后1年体重状况的变化，以体重指数标准差评分（BMI-SDS）表示。我们对来自全基因组关联研究的、位于以下基因内部或附近的肥胖风险单核苷酸多态性（SNP）进行基因分型：NEGR1、TNKS、SDCCAG8、FTO、MC4R、TMEM18、PTER、MTCH2、SH2B1、MAF、NPC1和KCTD15。
在干预期间，儿童的BMI-SDS降低（-0.28±0.35；p<0.001），而在干预结束至1年后BMI-SDS升高（+0.05±0.36；p=0.027）。包括NEGR1在内的所有SNP均与体重反弹无显著关联。
我们没有发现任何基于全基因组关联研究的肥胖标记等位基因在干预后1年内对体重反弹有影响的证据。
