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  • Hepatic lipase C-480T polymorphism modifies the effect of HDL cholesterol on the risk of acute myocardial infarction in men: a prospective population based study

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Hepatic lipase C-480T polymorphism modifies the effect of HDL cholesterol on the risk of acute myocardial infarction in men: a prospective population based study
  1. Y M Fan1,
  2. J T Salonen2,
  3. T A Koivu3,
  4. T-P Tuomainen4,
  5. K Nyyssönen5,
  6. T A Lakka6,
  7. R Salonen7,
  8. K Seppänen7,
  9. S T Nikkari8,
  10. E Tahvanainen9,
  11. T Lehtimäki10
  1. 1Department of Clinical Chemistry, Tampere University Hospital, Finland
  2. 2Research Institute of Public Health and Department of Public Health and General Practice, Kuopio, Finland
  3. 3Department of Clinical Chemistry, Tampere University Hospital, and Department of Medical Biochemistry, University of Tampere, Finland
  4. 4Research Institute of Public Health and Atherosis Research Unit, University of Kuopio, Finland
  5. 5Research Institute of Public Health, University of Kuopio, Finland
  6. 6Pennington Biomedical Research Centre, Louisiana State University, USA
  7. 7Research Institute of Public Health, University of Kuopio, Finland
  8. 8Department of Medical Biochemistry, University of Tampere, Finland
  9. 9Department of Medical Genetics, University of Helsinki, Finland
  10. 10Department of Clinical Chemistry, Tampere University Hospital, Finland
  1. Correspondence to:
 T Lehtimäki
 Laboratory of Atherosclerosis Genetics, Department of Clinical Chemistry, Centre for Laboratory Medicine, Tampere University Hospital, PO Box 2000, FIN-33521, Tampere, Finland; blteleuta.fi

https://doi.org/10.1136/jmg.2003.010652

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    Previous studies have revealed an inverse association between high density lipoprotein cholesterol (HDL-C) levels and the risk of acute myocardial infarction (AMI).1,2 HDL-C level is modulated by genetic factors as well as environmental factors such as obesity, smoking, and physical exercise. Hepatic lipase (HL) is a lipolytic enzyme in lipoprotein metabolism, functioning as a phospholipase, an acylglycerol hydrolase, and a ligand of cell surface glycosaminoglycans, hydrolysing triglyceride-rich lipoprotein particles.3 Recently, it has been reported that HL is synthesised by macrophages.4 The HL gene variation has a significant effect on the variability of HDL-C in the population.5,6 The functional HL promoter C-480T transition, also referred to as (-514C/T), leads to three common genotypes: CC, CT, and TT. The C and T alleles are associated with high and low HL activity, respectively.7–9 However, the common polymorphisms of HL (-480T), cholesterol ester transfer protein (CETP) (TaqIB), lipoprotein lipase (S447X), and lecithin cholesterol acyl transferase (S208T) contribute only about 2.5% to the variance of HDL-C in the population.10 This suggests that the HL C-480T polymorphism and HDL-C levels are different factors, and studying their interaction is justified. One previous study has shown that there might be an interaction between CETP gene polymorphism and HDL-C on the risk of myocardial infarction.11 This result raises the possibility that other polymorphisms associated with HDL-C—for example, HL gene polymorphism—might interact with HDL-C and thus modify the risk of AMI. In fact, an effect of the C-480T polymorphism on coronary artery disease (CAD) has been sought in several studies with both negative7,12 and positive findings.13–15 One possible reason for the mixed results may be the interaction between HL C-480T genotype and HDL levels on CAD, a hypothesis not studied previously. To address this question, and …

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