FADS1 Genes Expressed And Methylation Status Researched In The Rat Model With Hypertriglyceridemia

Objective To il ustrate the potential mechanisms of FADS1 on hepatic lipid metabolism with hypertriglyceridemia, we investigated the expression and Cp G island methylation of FADS1 in the BRL-3A liver cel s and the rat liver with hypertriglyceridemia in this study.Method The male Sprague–Dawley(SD) rats were fed with high fat diets(HFD) 3-5 weeks to reproduce the model with hypertriglyceridemia, and the BRL-3A liver cel s were treated with appropriate concentration of the medical fat emulsion to establish hypertriglyceridemia cell models. Quantitative real-time PCR and enzyme linked immunosorbent assay were used to analyze the expression of FADS1 in control group, hypertriglyceridemia group and treatment group(treated with 5-Aza-Cd R). The DNA methylation level was analyzed by cloning and sequencing. Furthermore, the methylated plasmids(p GL3-FADS1-M and p GL3-FADS1-U) generated by incubating plasmid DNA with Sss I methylase were transfected into BRL-3A liver cel s to research the effect of DNA methylation for FADS1 gene expression.Result The expression level of FADS1 in hypertriglyceridemia group was much lower than the control group. Compared with the hypertriglyceridemia cell group, FADS1 expression in the cell treated with 5-aza-Ad was increased. The methylation level at the FADS1 gene promoter region in hypertriglyceridemia group was higher than the control group, and was positive correlation with the serum triglyceride concentrations. Compared with the unmethylated group, the methylated group of fluorescence activity was decreased.Conclusion 1. The male SD rats fed with high fat diets can produce the rat model with hypertriglyceridemia, and the BRL-3A liver cel s treated with the medical fat emulsion concentration of 6% can establish the hypertriglyceridemia cell models. 2. The lower level of expression and abnormal methylation of FADS1 were correlated withhypertriglyceridemia.