4.7 Article

Effects of fish meal replaced by methanotroph bacteria meal (Methylococcus capsulatus) on growth, body composition, antioxidant capacity, amino acids transporters and protein metabolism of turbot juveniles (Scophthalmus maximus L.)

Journal

AQUACULTURE
Volume 562, Issue -, Pages -

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ELSEVIER
DOI: 10.1016/j.aquaculture.2022.738782

Keywords

Scophthalmus maximus L; Methanotroph bacteria meal; Growth performance; Amino acids transport; Protein metabolism

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MBM can replace up to 30% dietary FM without significantly adverse effects on growth performance and health of turbot juveniles, but excessive substitution levels (80% and 100%) would compromise antioxidant capacity, liver health, and protein metabolism.
Methanotroph bacteria meal (MBM) is produced by the fermentation of Methylococcus capsulatus, which use methane as carbon source. To evaluate the potential of replacing dietary fish meal (FM) with MBM, an eight -week growth trial was conducted on turbot juveniles (Scophthalmus maximus L.) with initial average weight of 9.13 +/- 0.02 g. Seven isonitrogenous (crude protein, 51.00%) and isolipidic (crude lipid, 11.50%) diets were formulated by substituting FM protein with 0% (MBM0, the control diet), 15% (MBM15), 30% (MBM30), 45% (MBM45), 60% (MBM60), 80% (MBM80) and 100% (MBM100) MBM. Each diet was randomly assigned to triplicate fibreglass tanks (600 L). The survival rate (over 98%) was not significantly different among dietary treatments (P > 0.05). Also, no significant differences in specific growth rate (SGR), feed efficiency ratio (FER) and flesh yield (FY) were observed among fish fed with diets MBM0, MBM15 and MBM30, whereas these pa-rameters were significantly reduced by further increase of dietary MBM (P < 0.05). Apparent digestibility co-efficient (ADC) of nutrients was significantly liner reduced with increasing dietary MBM (P < 0.05). The body composition was altered by dietary MBM, as evidenced by an increase in carcass ash and muscle palmitic acid (C16:0) proportion, along with a decrease in n-3 polyunsaturated fatty acids (PUFA) proportion in muscle. The antioxidant capacity was not compromised until the replacement level reached 80%, characterized by a signif-icant decrease in serum total antioxidant capacity (T-AOC), superoxide dismutase (SOD) activity and an increase in malondialdehyde (MDA) content. The liver health also tended to be compromised in fish fed with diets MBM80 and MBM100, evidenced by significantly increased glutamic oxalacetic transaminase (GOT) in serum and severe vacuolation of liver. The gene expression of intestinal amino acids transporters and hepatic general control nonderepressible 2 (gcn2) was first up-regulated and then down-regulated with significantly quadratic pattern (P < 0.05). Also, the expression of genes related to protein degradation in muscle, such as calpain small subunit 1-like (capns1-like), autophagy related 4B cysteine peptidase (atg4b) and cathepsin-d, exhibited a similar trend. While the gene expression of myogenic regulatory factors in muscle, such as follistatin, myogenin and myosin light chain (mlc), was significantly reduced in groups MBM80 and MBM100 as compared with the control (P < 0.05), which resembled the expression of mammalian target of rapamycin (mtor) in liver. Overall, MBM can replace up to 30% dietary FM without significantly adverse effects on growth performance and health of turbot juveniles, but excessive substitution levels (80% and 100%) would compromise antioxidant capacity, liver health and protein metabolism.

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