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Hepatic lipase gene -514 C/T polymorphism and premature coronary heart disease

Juying Ji1, Carly E Herbison, Cyril D S Mamotte

  • 1Cardiovascular Genetics Laboratory, Royal Perth Hospital, Department of Medicine, University of Western Australia and the Western Australian Heart Research Institute, Australia.

Insights

The hepatic lipase -514 C/T gene variant is linked to altered plasma lipids and a higher risk of coronary heart disease (CHD) in males, potentially due to impaired lipoprotein metabolism.

Area of Science:

  • Genetics
  • Cardiovascular Disease Research
  • Lipid Metabolism

Background:

  • A common polymorphism in the hepatic lipase (HL) gene promoter, -514C/T, influences enzyme activity and plasma lipoprotein levels.
  • The association between this HL gene polymorphism and coronary heart disease (CHD) requires further investigation.

Purpose of the Study:

  • To investigate the relationship between the HL -514 C/T polymorphism and CHD in Caucasian subjects.
  • To examine the impact of the HL -514 C/T polymorphism on plasma lipid profiles in relation to CHD status.

Main Methods:

  • A case-control study involving 562 Caucasian CHD patients under 50 and 642 healthy Caucasian controls.
  • Genotyping for the HL -514 C/T polymorphism and analysis of plasma lipid levels (HDL-cholesterol, triglycerides, total cholesterol, LDL-cholesterol).

Main Results:

  • Male CHD patients exhibited a higher carrier rate for the -514 T allele (41%) compared to controls (33%), indicating a predisposition to CHD.
  • In male CHD patients, the T allele was associated with higher HDL-cholesterol and more frequent occurrence in those with high triglycerides.
  • A novel polymorphism (-592A/G) was identified, potentially leading to misclassification of -514 C/T genotypes.

Conclusions:

  • The T allele of the hepatic lipase -514 C/T polymorphism is associated with altered plasma lipid profiles.
  • The increased CHD risk in males with the -514 T allele may stem from impaired triglyceride-rich lipoprotein metabolism and reverse cholesterol transport.
Abstract

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