The effect of oxidized fish oil on lipid metabolism in Rhynchocypris lagowski Dybowski

Fish oil can not only provide energy for the growth and development of fish, but also constitute a variety of tissue and cellular structural components of fish. However, fish oil is easily oxidized in the process of feed processing, treatment and storage, which reduces the feed quality and threatens the health of fish. Therefore, the purpose of this study was to investigate the effects of different degrees of oxidation of fish oil in feed on fatty acid composition and lipid metabolism in hepatopancreas of Rhynchocypris lagowski Dybowski. Five diets containing five oxidation levels (0, 100, 200, 300 and 400 meq/kg) of fish oil were formulated and fed to 525 healthy R. lagowski (4.48 +/- 0.14 g) that were randomly divided into 15 glass aquariums. After 8 weeks, hepatopancreas samples were taken for fatty acid composition, and biochemical analysis. The results showed that the content of Polyunsaturated fatty acid (PUFA) in muscle of R. lagowski increased significantly with the increase of oxidation degree of fish oil (P< 0.05), but there were no changes in Saturated fatty acid (SFA), Monounsaturated fatty acid (MUFA), EPA (C20:5n3), and Sn-6 (P> 0.05). Compared with the control group, the contents of SFA, MUFA and EPA in hepatopancreas were significantly increased (P< 0.05), while DHA (C22:6n3), Sn-3, Sn-6, and PUFA were decreased (P< 0.05). Feeding with OFO increased hepatopancreas total cholesterol (TC), triacylglycerol (TG), HDL/LDL ratio, FAS, and ACCa that involved in lipid synthesis enzymes (P< 0.05), while reduced liver esterase (HL), fatty acyl-CoA synthetase (ACS), carnitine palmitoyltransferase (CPT-1) and hormone-sensitive triglyceride lipase alpha (HSL alpha) enzyme activity and gene expression that associated with lipid decomposition (P< 0.05). It is suggested that the adverse effects of dietary oxidized oil may be achieved by promoting fatty acid synthesis, inhibiting fatty acid oxidation, increasing fatty acid uptake by hepatopancreas and reducing the ability of TG to transport from hepatopancreas to extrahepatic tissues, thus inducing fat accumulation in hepatopancreatic cells and further affecting lipid metabolism in hepatopancreas.