Relationship between plasma HDL subclasses distribution and lipoprotein lipase gene HindIII polymorphism in

Shiyin Long1, Ying Tian, Rong Zhang

  • 1Apolipoprotein Research Unit, Department of Biochemistry and Molecular Biology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, 610041 Sichuan, PR China.

Insights

The 495TT genotype of the Lipoprotein Lipase (LPL) gene HindIII polymorphism is linked to altered high-density lipoprotein (HDL) subclasses in Chinese hyperlipidemic individuals, suggesting impaired cholesterol metabolism.

Area of Science:

  • Biochemistry
  • Genetics
  • Cardiovascular Science

Background:

  • High-density lipoprotein (HDL) subclasses play crucial roles in lipid metabolism and atherosclerosis.
  • Lipoprotein lipase (LPL) activity influences HDL cholesterol levels, and LPL gene polymorphisms may affect HDL subclass distribution.

Purpose of the Study:

  • To investigate the association between LPL gene HindIII polymorphism and HDL subclasses distribution in Chinese hyperlipidemic and normolipidemic subjects.
  • To determine if LPL gene polymorphism impacts HDL subclass profiles in the context of hyperlipidemia.

Main Methods:

  • Assayed LPL gene HindIII polymorphism using PCR-RFLP.
  • Determined relative apolipoprotein A-I (apoA-I) contents of HDL subclasses via two-dimensional gel electrophoresis and immunodetection.
  • Analyzed 173 hyperlipidemic and 155 normolipidemic subjects.

Main Results:

  • The 495TT genotype and T allele were most frequent in both groups.
  • Hyperlipidemic subjects showed a shift towards smaller HDL subclasses, with increased prebeta1-HDL, prebeta2-HDL, HDL3b, and HDL3a, and decreased HDL2a and HDL2b.
  • The 495TT genotype in hyperlipidemic individuals was associated with higher triglycerides, apoB100, and TG/HDL-C ratio, and altered HDL subclass levels.

Conclusions:

  • The 495TT genotype of LPL gene HindIII polymorphism is associated with altered HDL subclass distribution in Chinese hyperlipidemic populations.
  • This alteration involves a shift towards smaller HDL particles, potentially indicating weakened reverse cholesterol transport (RCT) and abnormal HDL maturation.
Abstract

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