The association of LRP6 rs2302685 (V1062I) polymorphism with the risk of hyperlipidemia in Iranian children and adolescents

Wnt signaling/LRP6 plays a critical role in metabolic syndrome and atherosclerosis, and variation in this pathway may lead to hyperlipidemia, nonalcoholic fatty liver disease, and coronary artery disease. In the present study, we investigated the effect of LRP6 rs2302685 (V1062I) on hyperlipidemia i...

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Veröffentlicht in:Annals of human genetics 2018-11, Vol.82 (6), p.382-388
Hauptverfasser: Montazeri‐Najafabady, Nima, Dabbaghmanesh, Mohammad Hossein, Mohammadian Amiri, Rajeeh
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Sprache:eng
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Zusammenfassung:Wnt signaling/LRP6 plays a critical role in metabolic syndrome and atherosclerosis, and variation in this pathway may lead to hyperlipidemia, nonalcoholic fatty liver disease, and coronary artery disease. In the present study, we investigated the effect of LRP6 rs2302685 (V1062I) on hyperlipidemia in Iranian children and adolescents. The population in this study consisted of 200 children (101 boys, 99 girls) aged 9–18 years old. Total cholesterol, high‐density lipoprotein (HDL), low‐density lipoprotein (LDL), non‐HDL cholesterol, and triglyceride levels were measured. Body composition was evaluated by the Hologic DXA system. PCR/restriction fragment length polymorphism was performed for LRP6 rs2302685 (V1062I) genotyping. Logistic regression analysis was done to find the association between LRP6 rs2302685 (V1062I) and categorized lipid parameters in the adjusted model for confounding factors (age, sex, and puberty). Individuals with the CC genotype showed significantly higher levels of cholesterol, triglycerides, LDL, and non‐HDL compared to the CT and TT genotypes. In modeling analysis, for categorized lipid parameters, a significant association was found between CC versus CT, and CC versus TT in terms of cholesterol, LDL, and non‐HDL. It seems that LRP6 rs2302685 (V1062I) variant carriers are associated with an increased risk of hyperlipidemia in Iranian children and adolescents.
ISSN:0003-4800
1469-1809
DOI:10.1111/ahg.12254