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LPL gene Pvu II polymorphism and hypertriglyceridemia: a meta-analysis involving 1,640 subjects

  • Li, Yan-yan (Department of Geriatrics, First Affiliated Hospital of Nanjing Medical University) ;
  • Zhou, Yan-hong (Department of Geriatrics, First Affiliated Hospital of Nanjing Medical University) ;
  • Gong, Ge (Department of Geriatrics, First Affiliated Hospital of Nanjing Medical University) ;
  • Geng, Hong-yu (Department of Geriatrics, First Affiliated Hospital of Nanjing Medical University) ;
  • Yang, Xin-xing (Department of Geriatrics, First Affiliated Hospital of Nanjing Medical University) ;
  • Wang, Xiang-ming (Department of Geriatrics, First Affiliated Hospital of Nanjing Medical University) ;
  • Zhou, Chuan-wei (Department of Geriatrics, First Affiliated Hospital of Nanjing Medical University) ;
  • Xu, Jian (Department of Geriatrics, First Affiliated Hospital of Nanjing Medical University) ;
  • Qian, Yun (Department of Geriatrics, First Affiliated Hospital of Nanjing Medical University)
  • Received : 2016.02.15
  • Accepted : 2016.06.15
  • Published : 2017.11.01

Abstract

Background/Aims: Although lipoprotein lipase (LPL) gene Pvu II polymorphism has been associated with an increased risk of hypertriglyceridemia (HT), there is no clear consensus within the scientific community. Methods: A meta-analysis of 1,640 subjects from six individual studies was conducted to better elucidate the potential relationship between the LPL gene Pvu II polymorphism and HT within the Chinese population. Pooled odds ratios (ORs) and their corresponding 95% confidence intervals (CIs) were evaluated by using fixed effect models. Results: Our analysis indicated a significant association between LPL gene Pvu II polymorphism and HT within the Chinese population under allelic (OR, 1.550; 95% CI, 1.320 to 1.830; $p=1.158{\times}10^{-7}$), recessive (OR, 0.540; 95% CI, 0.390 to 0.750; p = 0.0002), dominant (OR, 1.889; 95% CI, 1.501 to 2.377; $p=5.960{\times}10^{-8}$), homozygous (OR, 2.167; 95% CI, 1.531 to 3.067; $p=1.242{\times}10^{-5}$), heterozygous (OR, 1.810; 95% CI, 1.419 to 2.309; $p=1.842{\times}10^{-6}$), and additive genetic models (OR, 1.553; 95% CI, 1.320 to 1.828; $p=1.158{\times}10^{-7}$). Conclusions: Because LPL gene Pvu II restriction fragment length polymorphism polymorphism was associated with an elevated risk of HT, the P+ allele carriers of the LPL gene might be predisposed to HT.

Keywords

Acknowledgement

Supported by : National Natural Science Foundation of China, Nanjing Medical University

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