Soybean oil alleviates maternal conjugated linoleic acid dietary-induced hatchability decrease and embryo hepatic lipolysis in broiler breeders

Abstract

The objective of the present study was to determine the effect of maternal conjugated linoleic acid (CLA) and soybean oil (SO) dietary on egg hatchability and hepatic lipometabolism in chick embryos. Broiler breeders (36 wk, 3.56 ± 0.12 kg) were randomly assigned to 6 treatments (with 6 replicates per treatment and 25 broiler breeder hens and 1 rooster per replicate) and fed a diet with 0.5% SO (control), or a diet with either 0.5% CLA, or CLA plus 0, 2, 4, 6, or 8% SO for 8 wk, with natural mating. The results showed that 0.5% CLA reduced hatchability of fertile eggs (P < 0.0001), which was reversed by SO supplementation and fully recovered at 6% SO (linear, P < 0.0001; quadratic, P < 0.0001). Meanwhile, maternal CLA dietary decreased the mRNA expression level of malic enzyme, sterol regulatory element-binding protein-1c (SREBP-1c), fatty acid synthetase and acetyl-CoA carboxylase 1 (ACC1) (P < 0.05), and increased the expression of peroxisome proliferator-activated receptor α (PPARα), and carnitine palmitoyl transferase 1 (CPT1) (P < 0.05) in the embryonic liver on day 14 and 21. In addition, the protein expression level of phospho-ACC1, phospho-PPARα and CPT1 were increased by maternal CLA dietary (P < 0.05), and the protein expression of phospho-SREBP-1c was inhibited (P < 0.05), indicating that maternal CLA dietary reduced fatty acid (FA) synthesis and accelerated FA catabolism. Soybean oil addition diminished CLA-mediated fatty acid catabolism, via increasing the gene and protein expression of fatty acid synthesis (ME, SREBP-1c, FAS, ACC1) (Linear, P < 0.05) but decreasing that of fatty acid lipolysis (PPARα and CPT1) (Linear, P < 0.05). In conclusion, SO supplementation modulated maternal CLA dietary-induced loss in egg hatchability and hepatic lipolysis in embryo livers. The regulatory mechanism of maternal CLA and SO dietary in offspring lipometabolism might be related to SREBP-1c and PPAR-α signaling pathways.