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Background  Identification of interactions between epigenetic factors and treatments might lead to personalized intervention of diseases. This paper aims to examine the modification effect of fenofibrate therapy on the association of methylation levels and fasting blood triglycerides (TG), and the related biological pathways among methylation sites.    Results  Mixed-effects models were employed to assess pre- and posttreatment associations and drug modification effects simultaneously. Five cytosine-phosphate-guanine (CpG) sites were found to be associated with TG levels before and after the fenofibrate therapy: cg00574958, cg17058475, and cg01082498 on  CPT1A  gene, chromosome 11; cg03725309 on  SARS , chromosome 1; and cg06500161 on  ABCG1 , chromosome 21. In addition, fenofibrate therapy modified the methylation levels on the following 4 CpG sites: cg20015535 (gene  EGLN1 , chromosome 1); cg24870738 (gene  RNF220 , chromosome 1); cg06891775 (gene  LOC283050 , chromosome 10); and cg00607630 (gene  USP7 , chromosome 16). Further, gene set enrichment analysis (GSEA) identified cancer- and metabolism-related pathways that were associated with TG-related CpG sites.    Conclusions  We identified modification effects of fenofibrate on the associations between blood TG levels and several CpG sites. Pathway enrichment analysis indicated the alternations in some metabolism and cancer-related pathways. Our findings have important implications for future research in pharmacoepigenetics and personalized medicine.

Modification effect of fenofibrate therapy, a longitudinal epigenomic-wide methylation study of triglycerides levels in the GOLDN study