A 3‐hr experiment was conducted to investigate the effects of dietary myo‐inositol (MI) supplementation on survival, immune response and antioxidant abilities in Litopenaeus vannamei under acute hypoxia stress. Six practical diets were formulated with supplementation of graded levels (control group 0, 0.1, 0.2, 0.4, 0.8 and 1.6 g/kg dry diet) of MI and were randomly assigned to triplicate groups of L. vannamei (mean weight 0.40 ± 0.00 g) for 8 weeks. Ten healthy shrimp (final mean weight approximately 11–14 g) randomly selected from each tank were exposed to hypoxia stress after feeding trial. After 3‐hr acute hypoxia stress, survival of shrimp fed MI‐supplemented diets (except 0.1 and 0.4 g/kg diets) was significantly increased compared with the control group. Shrimp fed control diet had lower activities of alkaline phosphatase (AKP), acid phosphatase (ACP), total antioxidant capacity (T‐AOC) and glutathione peroxidase (GPX), and higher malondialdehyde (MDA) and protein carbonyl (PC) contents in hepatopancreas than those fed the MI‐supplemented diets. In addition, mRNA expression levels of heat shock protein 70 (Hsp70), catalase (CAT) and penaeidin were significantly differentially regulated in hepatopancreas. In summary, dietary MI supplementation may have a positive effect on improving resistance to acute hypoxia stress of L. vannamei.

The following study aimed to develop a fatty liver model in primary hepatocytes isolated from Atlantic salmon. In order to induce the fatty liver, oleic acid (OA) at 0.2 or 0.4 mM was used. Metformin, known to prevent and cure fatty liver in mammalian cells, was used at 1 or 10 mM for 24 hr before addition of OA to test possible prevention effect of metformin on the OA‐induced fatty liver phenotype. Cells grown in 0.2 mM OA did not increase the mean number of lipid droplets, while cells grown in 0.4 mM OA increased the number of lipid droplets within the liver cells (p < 0.0001). Metformin pretreatment prior to OA supplementation reduced the mean number of lipid droplets. Gene expression of ApoB100, CD36 and PPARa increased in cells treated with metformin and most so at 10 mM. On the other hand, gene expression of LXR, SREBP2 and CPT‐1 decreased at both concentrations of metformin, while OA treatment did not affect these genes. Gene expression of IL‐8 increased by 0.4 mM OA (p = 0.002). Metformin reduced the gene expression of IL‐8. Thus, metformin efficiently enhanced the expression of genes related to transport and oxidation of lipids in hepatic cells of salmon, but required higher concentrations of OA and metformin than those required in rodent models to increase and prevent lipid accumulation, respectively.