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N-3 fatty acids in Atlantic salmon diets alter liver gene expression, fatty acid metabolism and susceptibility to oxidative stress

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Kjetil Aune

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kjetil.aune@nofima.no

XIII International Symposium of Fish Nutrition and Feeding; Florianopolis, Brasil, 2008-05-01–2208-05-04

Kjær, Marte Avranden; Kjær, Marte Avranden; Todorcevic, Marijana; Torstensen, Bente; Torstensen, Bente Elisabeth; Vegusdal, Anne; Ruyter, Bente

Changes in dietary fatty acid (FA) profile may affect lipid metabolism in Atlantic salmon in many ways. Dietary vegetable oils have for instance been shown to decrease the FA ¿-oxidation capacity and affect several genes, among these FA desaturases, mitochondrial proteins, transcription factors, co-activators and signal transducers. In addition, high levels of eicosapentanoic acid (EPA, 20:5n-3) is shown to induce mitochondrial proliferation. The major aims of this study were firstly to investigate how increasing dietary levels of n-3 FAs affect salmon liver FA metabolism and expression of lipid regulatory genes. Secondly, to investigate how high level of EPA and docosahexanioc acid (DHA, 22:6n-3) may influence the susceptibility to oxidative stress. Triplicate groups of Atlantic salmon (90 g mean initial weight) were fed for 21 weeks on one of four diets supplemented with 23 % lipid. EPA and DHA levels varied from 10 % of total FAs in the diet based on rapeseed oil (RO) to 19 % in the diet based on fish oil (FO), and further to approximately 50 and 55 % in the DHA-enriched and EPA-enriched diets, respectively. The fish were fed on these diets until they reached a final average weight of 344 g. Increasing dietary levels of n-3 FAs led to increasing percentages of these FAs in liver lipids, ranging from 30 to 48 % of total liver FAs. Relatively more of the 18:3n-3 in the RO diet than 20:5n-3 in the EPA-enriched diet was found as 22:6n-3 in liver lipids. However, a major increase in the percentage of the elongation product 22:5n-3 was found in liver from the EPA fed fish. These data were supported by decreased expression of ¿5- and ¿6-desaturase genes with increasing dietary levels of EPA and DHA. The diet with the highest level of DHA affected several of the lipid regulatory genes. Expression of peroxisome proliferator-activated receptor (PPAR) _b, thFA _b-oxidation genes acyl-CoA oxidase (ACO) and carnitine palmitoyl-rnsferase (CPT) II and genes for the transport proteins fatty acid binding protein (FABP10) and fatty acid transport protein (FATP1) were all increased compared to the RO group. The membrane lipids of mitochondria and microsomes are easily susceptible to reactive oxygen species (ROS). Increasing dietary levels of EPA and DHA clearly decreased the percentage of major phospholipids (PLs) in mitochondrial and microsomal membranes. The percentage of cardiolipin (CL) was 3.1 in the mitochondrial membrane of the EPA group compared to 6.6 in the FO group. There were three times higher incidence of membrane damage and lack of mitochondrial ¿-oxidation capacity together with increased super oxide dismutase (SOD) and caspase-3 activity in the EPA and DHA groups compared to the FO and RO groups. Clearly, the presence of oxidised lipid may have harmful effects on mitochondrial function. These results reveal new elements in favour of greater sensitivity of n-3 FAs to peroxidation in fish.