Browsing by Author "Yan Liu"

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    Dietary magnesium improves growth, antioxidant capacity, ammonia tolerance and intestinal health of juvenile freshwater prawn, Macrobrachium nipponense
    (Elsevier, 2022-11-15) Youqin Kong; Zhili Ding; Shanshan Wei; Changle Qi; Yan Liu; Yixiang Zhang; Samwel Mchele Limbu; Jinyun Ye
    The present study evaluated the effects of magnesium (Mg) on growth, antioxidant capacity, intestinal morphology and ammonia nitrogen resistance in juvenile oriental river prawn, Macrobrachium nipponense. Six semipurified diets (crude protein 401.1 g kg−1 diet; crude lipid 88.7 g kg−1 diet) containing Mg levels of 1.1, 1.4, 1.6, 2.1, 2.8 or 4.5 g kg−1 were formulated. A total of 1080 healthy juvenile prawns (0.151 ± 0.003 g) were randomly stocked into eighteen 300 L tanks (100 × 80 × 60 cm), each tank with 60 prawns. Each experimental diet was fed to prawns in triplicate twice daily (08:00 and 17:00) for eight weeks. After the feeding trial, 20 prawns from each tank were challenged with 37 mg/L ammonia nitrogen for 96 h, and the hemolymph, hepatopancreas and muscle of the rest of the prawns were collected. Final biomass was higher in prawns fed diets containing 1.6 and 2.1 g Mg kg−1 compared with those fed the diet with 1.1 g kg−1. Higher alkaline phosphatase (ALP) activity was obtained in the serum of prawns fed the 2.1 and 2.8 g Mg kg−1 diets. The highest activities of hepatopancreas superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and total antioxidant capacity (T-AOC) were observed in prawns fed 1.6–2.8 g Mg kg−1 of feed, and the lowest hepatopancreas malondialdehyde (MDA) concentrations and serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities were found in these treatment groups. Similarly, the prawns fed diets with 1.6 and 2.1 g Mg kg−1 had significantly lower MDA concentrations and cumulative mortality and higher antioxidant enzyme activities after ammonia nitrogen exposure. The intestinal epithelial cells were closely attached to the membrane in prawns fed the 2.1 g Mg kg−1 diet, but they were partly detached in those fed the 1.1 and 4.5 g Mg kg−1 diets. The minimum dietary Mg supplementations of juvenile M. nipponense were determined to be 1.6, 1.9, 2.0 and 2.2 g kg−1 feed, respectively, using broken-line regression analysis based on the final biomass, SOD, ALT and ALP.
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    The reduction of lipid-sourced energy production caused by ATGL inhibition cannot be compensated by activation of HSL, autophagy, and utilization of other nutrients in fish. Fish Physiology and Biochemistry, 47: 173–188
    (Springer, 2021-02) Si-Lan Han; Yan Liu; Samwel Mchele Limbu; Li-Qiao Chen; Mei-Ling Zhang; Zhen-Yu Du
    The adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL)–mediated lipolysis play important roles in lipid catabolism. ATGL is considered the central rate-limiting enzyme in the mobilization of fatty acids in mammals. Currently, severe fat accumulation has been commonly detected in farmed fish globally. However, the ATGL-mediated lipolysis and the potential synergy among ATGL, HSL, and autophagy, which is another way for lipid breakdown, have not been intensively understood in fish. In the present study, we added Atglistatin as an ATGL-specific inhibitor into the zebrafish diet and fed to the fish for 5 weeks. The results showed that the Atglistatin-treated fish exhibited severe fat deposition, reduced oxygen consumption, and fatty acid β-oxidation, accompanied with increased oxidative stress and inflammation. Furthermore, the Atglistatin-treated fish elevated total and phosphorylation protein expressions of HSL. However, the free fatty acids and lipase activities in organs were still systemically reduced in the Atglistatin-treated fish, and the autophagy marker LC3 was also decreased in the liver. On the other hand, glycogenolysis was stimulated but blood glucose was higher in the Atglistatin-treated fish. The transcriptomic analysis also provided the hint that the protein turnover efficiency in Atglistatin-treated fish was likely to be accelerated, but the protein content in whole fish was not affected. Taken together, ATGL plays crucial roles in energy homeostasis such that its inhibition causes loss of lipid-sourced energy production, which cannot be compensated by activation of HSL, autophagy, and utilization of other nutrients.