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Simple Summary: As one of the essential mineral elements, manganese (Mn) is involved in maintaining the growth and physiological function of fish species. An optimal dietary level of manganese accelerated the growth, lipid metabolism, Mn accumulation, and antioxidant capacity of coho salmon. The dietary Mn requirement for post-larvae coho salmon was 17.35 mg kg−1 and 19.75 mg kg−1 according to the SGR and FCR, respectively. An optimal dietary level of manganese had a positive effect on the antioxidant capacity by scavenging free radicals in fish bodies. In addition, dietary Mn improved lipid metabolism, and the signaling pathway of PI3K/AKT/mTOR may be involved in regulating the activity of lipid metabolism enzymes. In this study, post-larval coho salmon Oncorhynchus kisutch (initial weight 0.37 ± 0.03 g) were fed with 6 experimental diets with increasing manganese (Mn) content (2.4, 8.5, 14.8, 19.8, 24.6, and 33.7 mg kg−1) for 12 weeks. Our results indicated that the feed conversion rate (FCR), specific growth rate (SGR), condition factor (CF), crude protein, moisture, crude lipid, ash, whole-body Mn, and vertebral Mn were affected by the elevation of Mn content in the diet. The activities of hepatic GSH-PX, Mn-SOD, and CAT were enhanced with increasing Mn content in the diet and reached the highest value at 19.8 mg kg−1 Mn. However, the level of hydrogen peroxide (H2O2), superoxide anion (O2·−), and malondialdehyde (MDA) was reduced with increasing Mn content in the diet. In addition, the activity of hepatic lipase (HL) and lipoprotein lipase (LPL) was increased with the elevation of dietary Mn content and reached a peak value at 14.8 mg kg−1 Mn. The activity of fatty acid synthetase (FAS) and the content of nonesterified fatty acid (NEFA) were increased following the elevation of Mn content from 2.4 to 19.8 mg kg−1 in the diet. The results indicated that the appropriate dietary Mn supplementation improved the feeding efficiency, lipid metabolism, and antioxidant capacity of coho salmon. The dietary Mn requirement for post-larval coho salmon was 17.35 mg kg−1 and 19.75 mg kg−1 based on the SGR and FCR, respectively. An optimal dietary level of Mn enhances hepatic lipid metabolism, and the signaling pathway of PI3K/AKT/mTOR may be involved in regulating the activity of enzymes related to lipid metabolism. [ABSTRACT FROM AUTHOR]

• La accumulation affects nutrient elements content in the liver of zebrafish. • La affects hepatic lipid deposition via decreasing FAS, ACC, and ACL activity. • La affects wnt10b signaling pathway in the liver of zebrafish. • La may inhibit hepatic lipid deposition via wnt10b signaling in zebrafish. This paper investigates the effect of lanthanum (La) on lipid deposition and Wnt10b signaling in the liver of male zebrafish with exposure of 0, 10, 20, and 30 μmol/L La. It suggests that La can be accumulated in liver, and its treatments decrease the activities and gene expression of enzymes related to fatty acid synthesis. The levels of total cholesterol (TC), triglyceride (TG), and nonesterified fatty acids (NEFA) as well as the size of lipid droplets are decreased by La treatments. Moreover, La treatments affect the composition of fatty acids and the content of nutrient elements. Meanwhile, they also induce the gene expression of wnt10b, β-catenin, pparα , and pparγ , but inhibit gsk-3β gene expression in liver. Further study on the result of wnt10b gene interference shows that Wnt10b/β-catenin signaling plays a crucial role in the regulatory process of hepatic lipid deposition. Taken together, our observations suggest that La accumulation affects lipid deposition in the liver of male zebrafish, and Wnt10b signaling pathway may be involved in this process. [ABSTRACT FROM AUTHOR]

In this study, the mechanism by which GSK-3β regulates protein synthesis and lipid deposition was investigated in zebrafish (Danio rerio). The vector of pEGFP-N1-GSK-3β was constructed and injected into the muscle of zebrafish. It was found that the mRNA and protein expression of tuberous sclerosis complex 2 (TSC2) was significantly increased. However, the mRNA and protein expression of mammalian target of rapamycin (mTOR), p70 ribosomal S6 kinase 1 (S6K1), and 4E-binding protein 1 (4EBP1) was significantly decreased by the pEGFP-N1-GSK-3β vector in the muscle of zebrafish. In addition, the mRNA and protein expression of β-catenin, CCAAT/enhancer binding protein α (C/EBPα), and peroxisome proliferators-activated receptor γ (PPARγ) was significantly decreased, but the mRNA expression of fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), ATP-citrate lyase (ACL), and HMG-CoA reductase (HMGCR) was significantly increased by the pEGFP-N1-GSK-3β vector. The activity of FAS, ACC, ACL, and HMGCR as well as the content of triglyceride (TG), total cholesterol (TC), and nonesterified fatty acids (NEFA) were significantly increased by the pEGFP-N1-GSK-3β vector in the muscle of zebrafish. The content of free amino acids Arg, Lys, His, Phe, Leu, Ile, Val, and Thr was significantly decreased by the pEGFP-N1-GSK-3β vector. The results indicate that GSK-3β may participate in regulating protein synthesis via TSC2/mTOR signaling and regulating lipid deposition via β-catenin in the muscle of zebrafish (Danio rerio). [ABSTRACT FROM AUTHOR]