Lipid deposition in abalone Haliotis discus hannai affected by dietary lipid levels through AMPKα2/PPARα and JNK/mTOR/SREBP-1c pathway

Abstract

A 100-day feeding trial was conducted to investigate the effects of dietary lipid on growth performance and lipid deposition as well as the regulation mechanism in abalone Haliotis discus hannai Ino. Abalones (initial weight: 10.98 ± 0.05 g) were fed with graded levels of dietary lipid (1.57%, 2.34%, 3.17%, 3.82%, 4.63%, 5.56%, 6.17% and 6.72%). Results showed that weight gain rate (WGR) and increment in shell length of abalone were highest in 3.82% dietary lipid level. Based on the quadratic regression analysis for WGR, the optimal dietary lipid level for abalone was estimated to be 3.87%. Concentrations of the total triacylglycerol, low-density lipoprotein cholesterol and non-esterified fatty acids in serum as well as lipid contents in hepatopancreas and muscle were positively related to dietary lipid levels. Compared to the group with 3.82% of dietary lipid, higher (6.72%) and lower (1.57%) dietary lipid down regulated the expression of genes involved in fatty acids transport and lipolysis in hepatopancreas and muscle, which might be related to AMP-activated protein kinase α2 (AMPKα2)/peroxisome proliferator-activated receptor α (PPARα) signaling. Higher dietary lipid (6.72%) down regulated, while lower dietary lipid (1.57%) up-regulated the expressions of genes involved in de-novo lipogenesis in hepatopancreas. Both higher (6.72%) and lower (1.57%) dietary lipid down regulated these genes' expression in muscle. It was found that c-Jun N-terminal kinases (JNK)/mammalian target of rapamycin (mTOR)/sterol regulatory element-binding protein 1c (SREBP-1c) signaling participate in the regulation of de-novo lipogenesis. In conclusion, lipid deposition in abalone was affected by dietary lipid levels through AMPKα2/PPARα and JNK/mTOR/SREBP-1c pathway.