Clostridium autoethanogenum meal (CAM) is a novel single-cell protein, which is produced from bacteria using carbon monoxide (CO) as sole carbon source. To evaluate the efficiency of CAM as an alternative for dietary fish meal, a 56-days growth experiment was performed on juvenile turbot (Scophthalmus maximus L.) with initial average weight of 9.13 ± 0.02 g. Six iso-nitrogenous (crude protein, 51.0%) and iso-lipidic (crude lipid, 11.5%) diets were formulated with 0%, 15%, 30%, 45%, 60% and 80% dietary fish meal protein substituted by CAM protein, which were designated as CAM0 (the control group), CAM15, CAM30, CAM45, CAM60 and CAM80, respectively. Results showed that no significant differences were observed in survival rate (over 97.50%) among different dietary treatments (p > 0.05). The specific growth rate (SGR) was not significantly affected when replacement levels of dietary fish meal with CAM were less than 45% (p > 0.05). The feed intake (FI) was significantly linear reduced with increasing dietary CAM (p < 0.05), whereas no significant differences were observed in feed efficiency ratio (FER), protein efficiency ratio (PER) and protein retention (PR) among different dietary treatments (p > 0.05). With increasing dietary CAM, lipid retention (LR) and carcass lipid tended to be increased in both significantly linear and quadratic patterns (p < 0.05). The apparent digestibility coefficient (ADC) of crude protein and some essential amino acids, including threonine, valine, lysine, histidine and arginine, showed significantly linear increase with increasing dietary CAM (p < 0.05). Furthermore, with the increase of dietary CAM, the gene expression of intestinal peptide and amino acids transporters was first up-regulated and then down-regulated with significantly quadratic pattern (p < 0.05), peaking in fish fed with diets CAM30 or CAM45, which was similar to the expression of genes related protein degradation in muscle. For genes related to protein metabolism in liver and muscle, the expression of mammalian target of rapamycin (mtor) was not significantly affected by dietary CAM, while the general control nonderepressible 2 (gcn2) tended to be first up-regulated and then down-regulated with significantly quadratic pattern (p < 0.05). Apart from that, the lipid metabolism of turbot was also affected by high dietary CAM, evidenced by increased expression of hepatic genes related to lipogenesis as well as reduced expression of genes related to lipid oxidation and lipid transport. In conclusion, CAM can replace up to 45% fish meal protein in diet for juvenile turbot without significantly adverse effects on growth performance. But excessive dietary CAM would result in significant growth reduction, and excessive lipid deposition may also occur in fish fed diets with high levels of CAM.
Three 56-day feeding trials were conducted to evaluate dietary lipid requirements and effects of dietary lipid levels on growth, digestive enzyme activities, antioxidant capacity, and lipid metabolism in turbot (Scophthalmus maximus L.) at three growth stages. The initial mean body weight of turbot was 9.13 ± 0.17 g, 50.10 ± 0.38 g, and 80.05 ± 0.76 g (small, medium, and large turbot), respectively. Five practical diets were formulated to contain 68.4, 93.9, 120.7, 147.8, and 171.2 g/kg lipid (L68.4, L93.9, L120.7, L147.8, and L171.2), respectively. Results of three trials showed that the weight gain rate and specific growth rate of turbot fed with L120.7, L147.8, and L171.2 diets were all significantly higher compared with turbot fed with L68.4 and L93.9 diets except for large turbot fed with the L147.8 diet. Activities of intestinal trypsin, lipase and hepatic catalase, superoxide dismutase, and total antioxidant capacity firstly increased and then decreased as dietary lipids increased. Meanwhile, malondialdehyde content decreased firstly but then increased with the elevation of dietary lipids in small and medium turbot, and it was significantly higher in the L171.2 group than the rest in large turbot. With increasing levels of dietary lipid, contents of whole-body lipid, liver lipid, serum total cholesterol, triglyceride, and low-density lipoprotein cholesterol were markedly increased at three stages. In addition, serum high-density lipoprotein cholesterol contents increased firstly and then decreased over the L120.7 group. Transcriptional levels of lipolysis-related genes lipin1 and lpl were significantly upregulated firstly and subsequently downregulated with increasing dietary lipid levels except lipin1 in medium fish. Meanwhile, a significant increase in lipogenesis-related genes lxr and pparγ expressions was detected in all fish. Based on the specific growth rate, the dietary lipid level of 130.1, 120.1, and 107.7 g/kg was optimal for the growth performance of turbot cultured at three phases, respectively. Additionally, the results indicated that high lipid diets may lead to abnormal lipid deposition and affect the physiological health of turbot.
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