Dietary l-carnitine regulates liver lipid metabolism via simultaneously activating fatty acid ß-oxidation and suppressing endoplasmic reticulum stress in large yellow croaker fed with high-fat diets.

Dietary l-carnitine (LC) is a nutritional factor that reduces liver lipid content. However, whether dietary LC can improve lipid metabolism via simultaneous activation of mitochondrial fatty acid (FA) ß-oxidation and suppression of endoplasmic reticulum (ER) stress is still unknown. Large yellow croaker were fed with a high-fat diet (HFD) supplemented with dietary LC at 0, 1·2 or 2·4 ‰ for 10 weeks. The results indicated that a HFD supplemented with LC reduced the liver total lipid and TAG content and improved serum lipid profiles. LC supplementation administered to this fish increased the liver antioxidant capacity by decreasing serum and liver malondialdehyde levels and enhancing the liver antioxidant capacity, which then relieved the liver damage. Dietary LC increased the ATP dynamic process and mitochondrial number, decreased mitochondrial DNA damage and enhanced the protein expression of mitochondrial ß-oxidation, biogenesis and mitophagy. Furthermore, dietary LC supplementation increased the expression of genes and proteins related to peroxisomal ß-oxidation and biogenesis. Interestingly, feeding fish with LC-enriched diets decreased the protein levels indicative of ER stress, such as glucose-regulated protein 78, p-eukaryotic translational initiation factor 2a and activating transcription factor 6. Dietary LC supplementation downregulated mRNA expression relative to FA synthesis, reduced liver lipid and relieved liver damage through regulating ß-oxidation and biogenesis of mitochondria and peroxisomes, as well as the ER stress pathway in fish fed with HFD. The present study provides the first evidence that dietary LC can improve lipid metabolism via simultaneously promoting FA ß-oxidation capability and suppressing the ER stress pathway in fish.

[Residual level and ecological risk assessment of OCPs and PCBs in sediments of mudflat shellfish culturing areas in Ningbo, Zhejiang Province of East China].

GC-ECD methods were adopted to determine the residual level of OCPs (including HCHs and DDTs) and PCBs in the surface sediments collected from mudflat shellfish culturing areas in Ningbo, with the sources of the OCPs and PCBs analyzed and the ecological risks of the residual OCPs and PCBs evaluated. The residual level of OCPs was 0.80-32.40 ng X g(-1), and that of PCBs was 3.20-33.33 ng X g(-1). The HCHs mainly came from long distance atmospheric transportation and historical residues, while the DDTs had new input at some sites, possibly coming from the application of dicofol. At most sites, there existed potential ecological risks of p, p'-DDT and DDTs, with strong indications in Qiangtou and Xidian where the residual level of p, p'-DDT was higher than the effect rang median (ERM), suggesting an ecological menace to the benthos. The residual PCBs at most sites were in low level ecological risk.