Fatty liver disease is regularly observed in cultured large yellow croaker, and the disease leads to lower growth rates and reduced harvest yields. The goal of this study was to achieve a more detailed understanding of the physiological and molecular changes in response to high‐fat diet‐induced fatty liver in large yellow croaker. Large yellow croaker fed a high‐fat diet (HFD) for 9 weeks developed hepatic steatosis characterized by histological observation and significantly increased plasma triglyceride levels and serum alanine aminotransferase (ALT) activities. However, no significant differences in serum total protein, glucose, cholesterol, non‐esterified free fatty acids (NEFA), aspartate aminotransferase, high‐density lipoprotein and low‐density lipoprotein were observed between the normal diet and the high‐fat diet (HFD) group. The fatty acid composition of tissue lipids was not affected significantly by dietary lipid levels. Gene expression analysis demonstrated that the HFD decreased fatty acid synthase expression and increased PPARγ expression, but had no effect on lipoprotein lipase and PPARα expression. These results suggest that the HFD‐induced physiological changes and fatty liver may be due to the alteration of related gene expression. As such, further investigations of the metabolic pathways and differentially expressed genes are of particular significance in the mechanistic study and understanding of HFD‐induced fatty liver disease.

A 9-week feeding trial was conducted to investigate the impact of dietary lipid sources on the lipid mechanisms of large yellow croaker by feeding three isonitrogenous and isoenergetic diets containing ¢sh oil (FO), soybean oil (SO) and beef tallow (BT) respectively. The e¡ects of the diets on the growth performance, somatic indices, tissue fatty acid composition, histological changes and peroxisome proliferator-activated receptor (PPAR)g expression were evaluated. Experimental diets were all well accepted by ¢sh and no signi¢cant (P40.05) di¡erences were found in the weight gain, growth rate and feed conversion rate. The fatty acid pro¢le of the ¢sh ¢llet and liver re£ected the fatty acid composition of the diets. Speci¢c-fatty acids were selectively retained, however, in the £esh of the ¢sh; in particular, docosahexaenoic acid and arachidonic acid concentrations were higher than the dietary concentrations. When FO was replaced by SO or BT diets, the reduction in eicosapontaenoic acid in ¢sh tissue was more pronounced, suggesting a preferred utilization of this fatty acid. The consumption of SO displayed intense lipid accumulation in the liver of the ¢sh. The expression of PPARg increased signi¢cantly in the SO group compared with the FO and BT groups (Po0.05).

The gene encoding the VP28 envelope protein of White spot syndrome virus (WSSV) was cloned into expression vector pET-30a and transformed into the Escherichia coli strain BL21. After induction, the recombinant VP28 (rVP28) protein was purified and then used to immunize Balb/c mice for monoclonal antibody (MAb) production. It was observed by immuno-electron microscopy the MAbs specific to rVP28 could recognize native VP28 target epitopes of WSSV and dot-blot analysis was used to detect natural WSSV infection. Competitive PCR showed that the viral level was approximately 10(4) copies/mg tissue in the dilution of gill homogenate of WSSV-infected crayfish at the detection limit of dot-blot assay. Our results suggest that dot-blot analysis with anti-rVP28 MAb could rapidly and sensitively detect WSSV at the early stages of WSSV infection.

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