Interaction between Sex and LDLR rs688 Polymorphism on Hyperlipidemia among Taiwan Biobank Adult Participants

Biomolecules. 2020 Feb 5;10(2):244. doi: 10.3390/biom10020244.

Abstract

Hyperlipidemia is one of the strong risk factors for ischemic heart disease. Using the Taiwan Biobank (TWB) database, we evaluated the risk of hyperlipidemia and its interaction with sex and rs688 polymorphism on the low-density lipoprotein receptor (LDLR) gene. Data collection in the biobank started in 2008 and is ongoing. Data analysis was performed on the participants' data collected between 2008 and 2015. In general, 27.92% of the 9237 female participants and 32.65% of the 8690 male participants were identified with hyperlipidemia. Compared to the C/C genotype, C/T and T/T genotypes were not significant risk factors for hyperlipidemia (OR = 1.061, CI: 0.976-1.153 for C/T and OR = 1.052, CI: 0.845-1.309 for T/T genotype) in the general model. However, there was a significant interaction between sex and rs6888 on hyperlipidemia risk (p-interaction = 0.0321). With the male sex/CC genotype being the reference group, only the female sex/CT and T/T genotypes were closely associated with hyperlipidemia, with respective ORs of 1.153 (CI: 1.014-1.311) and 1.423 (CI: 1.056-1.917). Our data indicate that rs688 C/T and T/T genotypes may be associated with increased risk of hyperlipidemia in Taiwanese women. These findings may be relevant in lipid-modification therapy.

Keywords: biobank; hyperlipidemia; polymorphism; sex.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Biological Specimen Banks
  • Female
  • Genetic Predisposition to Disease
  • Genotype
  • Humans
  • Hyperlipidemias / epidemiology*
  • Hyperlipidemias / genetics*
  • Male
  • Middle Aged
  • Myocardial Ischemia / epidemiology
  • Myocardial Ischemia / genetics
  • Odds Ratio
  • Polymorphism, Single Nucleotide*
  • Receptors, LDL / genetics*
  • Risk
  • Sex Factors*
  • Taiwan / epidemiology
  • Taiwan / ethnology

Substances

  • LDLR protein, human
  • Receptors, LDL