As the global demand for aquafeed ingredients continues to rise, sourcing sustainable alternatives is crucial for aquaculture industries. This study aimed to explore the potential of enzymatic hydrolysate as a substitute for traditional fishmeal and soybean meal in diets for juvenile sea cucumbers (Apostichopus japonicus). Three isonitrogenous (15% crude protein) and isolipidic (2.4% crude lipid) diets were formulated: a control diet containing 10% fishmeal and 5% soybean meal and two experimental low-fishmeal (8%) and low-soybean meal (0%) diets, supplemented with either 8% enzymatically hydrolyzed fish stickwater (EFS) or 8% enzymatically hydrolyzed chicken pulp (ECP), designated as Control, EFS, and ECP, respectively. Juvenile sea cucumbers (initial body weight, 0.25 ± 0.01 g) were fed these diets for 84 days to evaluate the effects of ECP and EFS on their growth performance, antioxidant capacity, and inflammatory responses. The results revealed significantly higher final weights and specific growth rates in both experimental groups than the control (p < 0.05). The proximate chemical compositions of sea cucumber were less affected by the diets (p > 0.05). Compared with the control group, significantly elevated levels of digestive enzymes, antioxidants, and lysozyme, together with lower malondialdehyde levels, were recorded in the experimental groups (p < 0.05). ECP appeared to exhibit greater potency than EFS in enhancing growth performance and antioxidant capacity. Similar trends were observed in the mRNA expression of SOD, CAT, and inflammation-related genes across the groups. In a nutshell, both ECP and EFS supplemented in a low-fishmeal and low-soybean meal diet could effectively promote the growth and health of A. japonicus, with ECP showing a superior effect over EFS. These findings suggest that enzymatic hydrolysate demonstrates potential as a viable alternative to traditional fishmeal and soybean meal in diets for sustainable sea cucumber aquaculture. Further investigations are warranted to reveal its underlying mechanism.
This study evaluated the effects of dietary phospholipid (PL) source and supplementation level on growth performance, antioxidant capacity, and lipid metabolism in Atlantic salmon (Salmo salar) fry. A 56-day feeding trial was conducted using a basal diet containing 1.76% PL and six experimental diets with an additional 1.5%, 3.0%, or 4.5% PL provided by soybean lecithin (SL) or krill oil phospholipids (KOP). Dietary supplementation with 3.0–4.5% SL and 1.5–4.5% KOP significantly improved growth performance, whereas feed conversion ratio was significantly reduced in the 3.0–4.5% SL and 3.0% KOP groups (p < 0.05). At equivalent inclusion levels, no significant differences were observed between SL and KOP in growth performance parameters (p > 0.05). PL supplementation also reduced whole-body lipid deposition and enhanced visceral lipase activity in all groups except the 1.5% SL group, while antioxidant capacity was improved in all PL-supplemented groups (p < 0.05). SL had no significant effect on whole-body fatty acid composition (p > 0.05), whereas moderate to high levels of KOP significantly altered the fatty acid profile, characterized by reduced monounsaturated fatty acids and n-6 polyunsaturated fatty acids, along with increased eicosapentaenoic acid (EPA) levels (p < 0.05). Transcriptomic analysis indicated that PL supplementation affected hepatic lipid metabolism, with both PL sources downregulating apoa2-like, while KOP induced stronger hepatic transcriptional responses related to lipid utilization and innate immune signaling than SL (padj < 0.05). However, gut microbiota analysis revealed no significant differences in the relative abundances of the dominant phyla or in α- and β-diversity among the control, 3.0% KOP, and 4.5% SL groups (p > 0.05). Overall, dietary PL supplementation promoted growth, improved antioxidant capacity, enhanced lipid metabolism, and reduced lipid deposition in Atlantic salmon fry, with KOP exerting stronger effects than SL on fatty acid composition and hepatic gene expression.