Why the study?
Are Lipoprotein lipase gene polymorphisms associated with coronary artery disease in the Korean population?
Are Lipoprotein lipase gene polymorphisms associated with coronary artery disease in the Korean population?
LPL gene polymorphisms (PvuII, HindIII, Ser447Ter) are not directly associated with CAD in the Korean population, but they do influence lipid profiles and BMI.
LPL polymorphisms should not guide CAD risk assessment in Koreans; leaves open their lipid effects in established disease.
Background:The accumulation of lipoprotein and monocyte in the intima of the arterial wall is the most important step of the development of coronary artery disease (CAD).Lipoprotein lipase (LPL) plays an antiatherogenic role by lipolysis of triglyceride-rich lipoproteins, but, it may also act as a receptor of some lipoproteins and monocyte at the arterial wall and act as a atherogenic molecule.Previous studies showed somewhat contradictory results about the association of CAD and LPL polymorphisms and mutations.Racial and dietary difference may contribute to these contradictory results.In this study, we tried to find out the association of CAD and the genetic variation of the LPL (PvuⅡ RFLP in intron 6, HindⅢ RFLP in intron 8 and Ser 447 Ter mutation in exon 9) in Korean population.Method and Result:CAD patients (n=146), confirmed by coronary angiography and healthy Korean adult volunteers (n=110) were genotyped for PvuⅡ /HindⅢ RFLP and Ser447Ter mutation of the LPL gene by PCR-digestion method.Between two groups, the genotype frequency of these genetic variations was not different.But, the genetic variations showed different effect on lipid profile and body mass index (BMI) in the CAD group and in the control group.In the CAD group, P1 allele carriers showed higher total cholesterol (P1P1+P1P2:P2P2=216±51 mg/dl:198±38 mg/dl, p=0.039) and higher LDL cholesterol level (P1P1+P1P2:P2P2=143±46 mg/dl:126±36 mg/dl, p=0.047), and H1 allele carriers had lower Body mass index than non-carriers (23.8±2.3 kg/m 2 :24.8±2.9 kg/m 2 , p=0.047).In the control group, the Ser447Ter mutation carriers had higher HDL cholesterol level than non-carriers (59±10mg/dl versus 53±11mg/dl, p=0.049) and patients with P1 allele showed lower body mass index (P1P1+P1P2:P2P2=23.1±2.6 kg/m 2 :24.5±2.6 kg/m 2 , p=0.006).Conclusion:In Korean, PvuⅡ/HindⅢ RFLP and Ser447Ter mutation was not associated with CAD, and they showed different effect on the lipid profile and on the body mass index according to the study group.
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Park et al. (1999) studied this question.
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