Fish are highly nutritious components of the human diet and the main source of essential n 3 long chain polyun saturated fatty acids. The beneficial effects of fatty acids, such as eicosapentaenoic acid and docosahexaenoic acid, are numerous and import ant, including protection against a range of cardiovascu lar and inflammatory diseases, as well as neurological disorders. Atlantic salmon can grow well on diets where FO has been completely replaced by VO but this results in lower levels of n 3 LC PUFA in their flesh, compromising their nutritional value and health promoting effects to the human consumer. The use of selective breeding programs to enhance traits of commercial importance is becoming increas ingly common in aquaculture.

It has been suggested Inhibitors,Modulators,Libraries that combining genetic selection for fish that are more efficient in retaining and or biosynthesising n 3 LC PUFA with changes in commercial diet formulations might be a viable strat egy to meet growing worldwide demands for aquaculture products, without loss of nutritional value. Previous studies have shown wide individual variability in the capacity of Atlantic salmon to retain or synthesize n 3 LC PUFA when fed Inhibitors,Modulators,Libraries VO diets. Following this, Leaver et al. demonstrated that deposition and or retention in flesh of dietary n 3 LC PUFA, EPA and DHA, is a highly heritable trait in salmon. These results have prompted further interest in large scale in depth studies exploring genotype �� nutrient interactions in sal mon, analysing whether the genetic background of the fish could affect the physiological response to complete dietary replacement of FO by VO.

In the present study we investigated this further by analyzing the tran scriptome from liver, the primary site of synthesis and export of lipids to extra hepatic tissues including flesh, from four Atlantic salmon families phenotyped for dif ferent levels of flesh n 3 LC PUFA content in response to GSK-3 a VO diet. The objective was to identify gene path ways and molecular mechanisms that might underlie differences in flesh n 3 LC PUFA contents when salmon families were fed the same low LC PUFA diet. Further more, because n 3 LC PUFA level is a component of, and associated with total lipid content in a tissue, a fac torial Inhibitors,Modulators,Libraries design was chosen in which families containing higher and lower proportions of flesh n 3 LC PUFA Inhibitors,Modulators,Libraries were compared at similar flesh total lipid contents. Results Family lipid contrasts Lipid analysis of fifty Atlantic salmon families showed flesh lipid levels ranging from 2. 3 to 5. 7% of wet weight, with relative and absolute n 3 LC PUFA contents vary ing from 71 to 136 and 314 to 554, respectively.