Interaction of common sequence variants and selected risk factors in determination of HDL cholesterol levels.

Clin Biochem

Institute of Biology and Medical Genetics, 1st Faculty of Medicine and General Teaching Hospital, Charles University in Prague, 12800 Prague, Czech Republic.

Published: June 2010

AI Article Synopsis

  • The study aimed to examine how certain genetic variants and their interactions influence HDL-c (high-density lipoprotein cholesterol) plasma levels in individuals with high triglyceride and LDL-c levels.
  • A total of 743 participants (340 men and 403 women) were analyzed, focusing on five specific genetic sites and their association with HDL-c levels using linear regression models.
  • The findings revealed that the CETP promoter variant significantly impacted HDL-c levels, while interactions between APOA1 genotype and menopause, as well as ABCA1 and APOE isoforms, also played important roles in affecting HDL-c concentrations.

Article Abstract

Objectives: The aim of our study was to assess the association of common sequence variants, and selected interactions, with HDL-c plasma levels.

Design And Methods: We analysed 743 individuals (340 men and 403 women) with high mean triglyceride and LDL-c levels. The association of five polymorphic sites (ABCA1 g.1051G>A, APOA1 g.-75G>A, CETP g.-629C>A, HNF1A g.102A>C, and LIPG g.584C>T), apoE isoforms and selected interactions with HDL-c levels were evaluated using linear regression models.

Results: After adjusting for triglycerides, sex, and BMI the only genotype with a statistically significant effect on HDL-c levels (p-value=0.004) was the CETP promoter variant. Further, linear regression model with interactions included indicated possible interplay between APOA1 genotype and menopause (p-value=0.002) and ABCA1 and APOE isoforms (p-value=0.017) on HDL-c plasma concentration.

Conclusions: Our study indicated that not only the CETP variant but also apoE isoforms and menopause could operate as potent modulators of HDL-c concentrations.

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Source
http://dx.doi.org/10.1016/j.clinbiochem.2010.04.001DOI Listing

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