Background: Fatty liver disease (FLD) is a serious public health problem that is rapidly increasing. Evidence indicates that the transcription factor EB () gene may be involved in the pathophysiology of FLD; however, whether polymorphism has an association with FLD remains unclear.
Objectives: To explore the association among polymorphism, gene-environment interaction, and FLD and provide epidemiological evidence for clarifying the genetic factors of FLD.
Methods: This study is a case-control study. Sequenom MassARRAY was applied in genotyping. Logical regression was used to analyze the association between polymorphism and FLD, and the gene-environment interaction in FLD was evaluated by multiplication and additive interaction models.
Results: (1) The alleles and genotypes of each single nucleotide polymorphism and haplotypes of in the case and control groups were evenly distributed; no statistically substantial difference was observed. (2) Logistic regression analysis indicated that polymorphism is not remarkably associated with FLD. (3) In the multiplicative interaction model, rs1015149, rs1062966, rs11754668 and rs2273068 had remarkable interaction with the amount of cigarette smoking. Rs1062966 and rs11754668 also had a considerable interaction body mass index and alcohol intake, respectively. However, no remarkable additive interaction was observed.
Conclusion: polymorphism is not directly associated with FLD susceptibility, but the risk can be changed through gene-environment interaction.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10461375 | PMC |
http://dx.doi.org/10.1177/00368504211043766 | DOI Listing |
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