Effects of dietary lipid on lipid metabolism, methylation and expression of PI3KCa in the ovary of yellow catfish (Pelteobagrus fulvidraco)

The present study was conducted to determine the potential mechanisms of dietary lipid level influencing lipid deposition in the ovary of yellow catfish Pelteobagrus fulvidraco. For this purpose, two experiments were designed. In vivo, yellow catfish were fed with three diets containing 6.98%, 11.34% and 15.41% of lipid levels. In vitro, the primary oocytes from yellow catfish were incubated with three fatty acid levels (0, 0.2 and 0.5 mmol/L), respectively. Triacylglyceride (TG) contents, methylation level of PI3KCa, and enzymes activities of FAS, G6PD, 6PGD, and ME, as well as the mRNA level of PI3KCa, DNMTs and other genes involved in lipid metabolism were determined in the ovary and oocytes of yellow catfish. GSI increased with increasing dietary lipid levels. Among three lipid treatments, TG content and the enzyme activities of FAS, G6PD, 6PGD, and ME, and mRNA expression of LPL and CD36 were highest in the 11.34% of dietary lipid level in the ovary; CPT IA mRNA expression was the highest for fish fed 15.41% dietary lipid; the lowest mRNA level of PI3KCa and the highest methylation percentage of PI3KCa promoter at -64 and -52 CpG sites were found in the 15.41% of dietary lipid group; Dietary lipid levels influenced the mRNA level of DNMT3b, but not the expression of DNMT1 and DNMT3a. DNMT3b mRNA expression was the highest in 15.41% of dietary lipid group, indicating that DNMT3b was more sensitive than DNMT1 and DNMT3a in response to dietary lipid level. In contrast, the in vitro study indicated that TG content, enzyme activities of FAS, G6PD and ME, and G6PD mRNA expression were the highest in the 0.5 mmol/L FA group, and mRNA expression levels of CPT IA, ACCb, LPL and CD36 were the highest in the control; FA incubation significantly increased the mRNA level of PI3KCa, reduced mRNA levels of DNMT1 and DNMT3b, but showed no significant effect on the methylation of PI3KCa promoter and on mRNA expression of DNMT3a.