Abstract
This study was conducted to obtain the optimal dietary lipid requirement and evaluate the differential regulatory effects of optimal or excessive dietary lipid levels on growth performance, lipid metabolism and physiological responses including oxidative stress (OS) and endoplasmic reticulum stress (ERS) of juvenile black seabream (Acanthopagrus schlegelii) (initial weight 2.08 ± 0.01 g). Six isonitrogenous experimental diets were formulated with graded levels of lipid: 6.87% (D1), 11.17% (D2), 14.35% (D3), 18.89% (D4), 23.93% (D5) and 26.94% (D6), respectively. Results indicated that fish fed with the D2 diet showed significantly higher values of final weight (FW), weight gain (WG) and specific growth rate (SGR) than those fed with the other diets, except for D3 group. In fish fed with the diets containing 11.17% and 14.35% (D2 and D3 groups) had the significantly higher contents of high density lipoprotein cholesterol (HDL-C) than other treatments, but showed markedly low concentrations of low density lipoprotein cholesterol (LDL-C). The contents of cholesterol (TC), triglyceride (TG), aspartate aminotransferase (AST) and alanine transaminase (ALT) in serum increased with the increasing of dietary lipid levels, except for the contents of AST and ALT in D1 group. Likewise, the results of hepatic paraffin section indicated that fish fed the dietary lipid levels of 18.89% or beyond (D4, D5 and D6) increased vacuolar fat drops and induced hepatic fat pathological changes. The mRNA expression level and protein concentration of sterol regulatory element-binding protein-1(srebp-1) were significantly up-regulated with the increasing of dietary lipid levels. However, the mRNA expression levels and protein concentrations of peroxisome proliferator-activated receptor alpha (pparα) and silent information regulator 1 (sirt1) significantly activated by fish fed with the D2 diet. Additionally, when fish fed with excessive dietary lipid (over 18.89%) could result in various responses related to OS and ERS. The key marker of OS malonaldehyde (MDA) was significantly increased with the increasing of dietary lipid levels being highest in the D6 group. A contrary pattern was found for total antioxidant capacity, which showed significantly higher activity in the D2 group. All parameters related to ERS increased with the increasing of dietary lipid levels and, hence, triggering inflammation and apoptosis by up-regulating the expression levels of key genes including nuclear factor kappa B (nf-κb) and c-Jun N-terminal kinase (jnk). Overall, based on WG, the optimal dietary lipid requirement of juvenile A. schlegelii is 12.82% by quadratic curve model analysis. When dietary lipid level exceeded 18.89%, excessive lipid could reduce growth performance, cause hepatic fat pathological changes, induce lipid deposition by modulating Sirt1/Srebp-1/Pparɑ pathways, lead to OS and ERS and, hence, triggering hepatic inflammation and apoptosis. These findings provide further insight and understanding of the regulatory effects on growth, lipid metabolism, physiological stress response (including OS and ERS) of A. schlegelii fed with optimal or excessive dietary lipid levels
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