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Int J Mol Sci ; 24(14)2023 Jul 11.
Artículo en Inglés | MEDLINE | ID: mdl-37511066

RESUMEN

Oxidative stress is one of the pillars crucial in the development of a non-alcoholic fatty liver disease (NAFLD) and may cause DNA damage. Since the main pathway responsible for the repair of oxidative DNA damage is the base-excision repair (BER) pathway, we examined the relationship between the presence of different genetic variants of BER-associated genes and the risk of NAFLD. The study evaluates seven single nucleotide polymorphisms (SNPs) within five genes, hOGG1, APEX1, NEIL1, LIG3, LIG1, in 150 NAFLD patients and 340 healthy controls. The genotyping was performed using TaqMan probes and the results were presented as odds ratio with its corresponding 95% confidence interval. The following SNPs were assessed in the study: hOGG1 (rs1052133), APEX1 (rs176094 and rs1130409), NEIL1 (rs4462560), LIG3 (rs1052536), LIG3 (rs4796030), and LIG1 (rs20579). Four of the investigated SNPs, i.e., rs176094, rs1130409, rs4462560 and rs4796030, were found to be associated with NAFLD risk. Furthermore, the occurrence of insulin resistance in patients with steatosis depended on various LIG3 genetic variants. The findings imply the impact of genes involved in BER on NAFLD and fatty liver-related insulin sensitivity.


Asunto(s)
ADN Glicosilasas , Enfermedad del Hígado Graso no Alcohólico , Humanos , Polimorfismo de Nucleótido Simple , Enfermedad del Hígado Graso no Alcohólico/genética , Predisposición Genética a la Enfermedad , Reparación del ADN/genética , Daño del ADN , Estudios de Casos y Controles , ADN Glicosilasas/genética
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