Department of Epidemiology and Biostatistics, Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, 87 Ding Jiaqiao Road, Nanjing 210009, China.
Eur J Pediatr. 2011 Oct;170(10):1309-16. doi: 10.1007/s00431-010-1355-8. Epub 2011 Mar 25.
Childhood obesity is increasingly prevalent in the community and is related to many adult diseases. Lipoprotein lipase (LPL) plays a central role in dyslipidemia, and polymorphisms of the LPL gene may result in the disturbance in the lipid's metabolism. The aim of this study is to test the hypothesis that genetic variants of LPL and serum lipid levels are associated with the risk of childhood obesity. We genotyped +495T > G and PvuII T > C in an LPL gene and measured the serum lipid levels in a case-control study of 124 obese children and 346 frequency-matched normal controls in preschool Chinese children. The variant genotypes of LPL + 495GG and PvuII CC were associated with a significantly increased risk of childhood obesity [adjusted odds ratio (OR) = 2.39, 95% CI = 1.09-5.23 for +495 GG; adjusted OR = 2.00, 95% CI = 1.04-3.83 for PvuII CC], compared with their wild-type genotypes, respectively. In addition, compared with the lower serum level cut off by the control median, the higher level of serum triglyceride (TG) (>0.59 mmol/L) was associated with a 1.32-fold increased risk of childhood obesity, and the higher level of high density lipoprotein cholesterol (HDLC) (>1.14 mmol/L) was associated with a 36% decrease in risk of childhood obesity. Furthermore, the median levels of TG were higher in obese children carrying LPL +495TT/TG and PvuII TT/CT genotypes than those in controls, the HDLC levels were lower in obese children carrying LPL +495TG and PvuII CT/CC genotypes than those in controls. In conclusion, the LPL gene +495T > G and PvuII T > C polymorphisms may modulate the magnitude of dyslipidemia in Chinese early-onset obesity.
儿童肥胖症在社区中越来越普遍，与许多成人疾病有关。脂蛋白脂肪酶（LPL）在血脂异常中起核心作用，LPL 基因的多态性可能导致脂质代谢紊乱。本研究旨在检验以下假说，即 LPL 基因的遗传变异和血清脂质水平与儿童肥胖的风险有关。我们在一个病例对照研究中对 124 名肥胖儿童和 346 名匹配频率的正常对照儿童的 LPL 基因中的+495T > G 和 PvuII T > C 进行了基因分型，并测量了血清脂质水平。LPL+495GG 和 PvuII CC 变异基因型与儿童肥胖的风险显著增加相关[调整后的优势比（OR）= 2.39，95%可信区间（CI）= 1.09-5.23 对于+495 GG；调整后的 OR = 2.00，95%CI = 1.04-3.83 对于 PvuII CC]，与野生型基因型相比。此外，与对照中位数截断的较低血清水平相比，血清三酰甘油（TG）水平较高（>0.59mmol/L）与儿童肥胖的风险增加 1.32 倍相关，而高密度脂蛋白胆固醇（HDLC）水平较高（>1.14mmol/L）与儿童肥胖的风险降低 36%相关。此外，携带 LPL+495TT/TG 和 PvuII TT/CT 基因型的肥胖儿童的 TG 中位数水平高于对照组，携带 LPL+495TG 和 PvuII CT/CC 基因型的肥胖儿童的 HDLC 水平低于对照组。总之，LPL 基因+495T > G 和 PvuII T > C 多态性可能调节中国早发性肥胖症血脂异常的程度。
