Association between the LXRα polymorphism and stroke in a Chinese population

Abstract

ABSTRACT. We examined the relationship between the liver X receptor α gene (LXRα) polymorphism and the susceptibility to stroke. We utilized the single fluorescent-labeled probe technique to detect the genotype of rs12221497 in the LXRα gene in 400 stroke patients and 400 healthy control subjects. The difference in genotype distribution between the 2 groups was analyzed using the chi-square test. Serum lipids and glucose levels between the different genotypes were also compared. We found that the risk of stroke in carriers with the AA + GA genotype was 2.02-fold higher than that in GG genotype carriers (odds ratio = 2.02, 95% confidence interval = 1.18-2.87, P < 0.05), and that the risk of stroke in carriers with the A allele increased by 0.606-fold compared to that in G allele carriers (odds ratio = 1.606, 95% confidence interval = 1.158-2.228). Logistic regression analysis showed that after adjusting for other confounding factors, the A allele 1758 J.S. Yang et al. ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (1): 1757-1762 (2015 was an independent risk for stroke. However, there were no differences in serum lipids and glucose levels between each genotype. We conclude that the rs12221497 polymorphism in the LXRα gene was associated with the susceptibility to stroke in a Han Chinese population.

Association of Drug-Metabolizing Enzyme and Transporter Gene Polymorphisms and Lipid-Lowering Response to Statins in Thai Patients with Dyslipidemia

“…Polymorphisms of genes that involve in the regulation of lipid metabolisms such as apolipoprotein E (apo E), cholesteryl ester transfer protein (CETP), and liver X receptors (LXR) have been reported to correlate with the efficacy of statin and susceptibility to cardiovascular disease. [6][7][8][9][10][11] Several studies have revealed that the genetic variants of the pharmacokinetics-related genes result in the diversity of statin efficacy among individuals. [12][13][14] Since statins have the primary site of action and metabolism in the liver, where they inhibit HMG-CoA reductase, the genetic variations of Phase I and II drug-metabolizing enzymes and drug transporter genes may have a critical role in the concentration of statins within hepatocytes and plasma, and consequently clinical efficacy to the treatment of statin.…”