Hovsepian Silva, Javanmard Shaghayegh Haghjooy, Mansourian Marjan, Hashemipour Mahin, Tajadini Mohamadhasan, Kelishadi Roya
Department of Pediatrics, Child Growth and Development Research Center, Research Institute for Primordial Prevention of Non-communicable Disease, Emam Hossein Children's Hospital, Isfahan, Iran.
Applied Physiology Research Center, Research Institute for Primordial Prevention of Non-communicable Disease, Isfahan University of Medical Sciences, Isfahan, Iran.
J Res Med Sci. 2018 Feb 20;23:11. doi: 10.4103/jrms.JRMS_911_17. eCollection 2018.
Genetically, predisposed children are considered as at-risk individuals for cardiovascular disease. In this study, we aimed to compare the frequency of four-lipid regulatory polymorphism in obese and normal-weight children with and without cardiometabolic risk factors.
In this nested case-control study, 600 samples of four groups of participants consisted of those with normal weight with and without cardiometabolic risk factors and obese with and without cardiometabolic risk factors. Allelic and genotypic frequencies of GCKR (rs780094), GCKR (rs1260333), MLXIPL (rs3812316), and FADS (rs174547) polymorphisms were compared in the four studied groups.
Data of 528 samples were complete and included in this study. The mean (standard deviation) age of participants was 15.01 (2.21) years. Frequency of tt allele (minor allele) of GCKR (rs1260333) polymorphism was significantly lower in normal weight metabolically healthy participants than metabolically unhealthy normal weight (MUHNW) and obese children with and without cardiometabolic risk factor ( = 0.01). Frequency of ga allele of GCKR (rs780094) polymorphism was significantly higher in normal weight children with cardiometabolic risk factor than in their obese counterparts with cardiometabolic risk factor ( = 0.04). Frequency of cg and gg alleles (minor type) of MLXIPL (rs3812316) polymorphism in normal weight metabolically healthy participants was significantly higher than MUHNW ( = 0.04) and metabolically healthy obese children ( = 0.04).
The findings of our study indicated that the minor allele of GCKR (rs1260333) single nucleotide polymorphisms (SNPs) could have pathogenic effect for obesity and cardiometabolic risk factors. Ga allele of GCKR (rs780094) SNPs had a protective effect on obesity. Minor alleles of MLXIPL (rs3812316) could have a protective effect for obesity and cardiometabolic risk factors.
从遗传学角度来看，具有遗传易感性的儿童被视为心血管疾病的高危个体。在本研究中，我们旨在比较有和没有心脏代谢危险因素的肥胖儿童与正常体重儿童中四种脂质调节多态性的频率。
在这项巢式病例对照研究中，600个样本分为四组参与者，包括有和没有心脏代谢危险因素的正常体重者，以及有和没有心脏代谢危险因素的肥胖者。比较了四组研究对象中GCKR（rs780094）、GCKR（rs1260333）、MLXIPL（rs3812316）和FADS（rs174547）多态性的等位基因和基因型频率。
528个样本的数据完整并纳入本研究。参与者的平均（标准差）年龄为15.01（2.21）岁。正常体重且代谢健康的参与者中，GCKR（rs1260333）多态性的tt等位基因（次要等位基因）频率显著低于代谢不健康的正常体重者（MUHNW）以及有和没有心脏代谢危险因素的肥胖儿童（P = 0.01）。有心脏代谢危险因素的正常体重儿童中，GCKR（rs780094）多态性的ga等位基因频率显著高于有心脏代谢危险因素的肥胖儿童（P = 0.04）。正常体重且代谢健康的参与者中，MLXIPL（rs3812316）多态性的cg和gg等位基因（次要类型）频率显著高于MUHNW（P = 0.04）和代谢健康的肥胖儿童（P = 0.04）。
我们的研究结果表明，GCKR（rs1260333）单核苷酸多态性（SNP）的次要等位基因可能对肥胖和心脏代谢危险因素具有致病作用。GCKR（rs780094）SNP的ga等位基因对肥胖具有保护作用。MLXIPL（rs3812316）的次要等位基因可能对肥胖和心脏代谢危险因素具有保护作用。
