The first salmon trials in Scotland involved feeding post-smolts diets containing FO and where FO was replaced by 25, 50, 75 & 100% linseed oil (LO) plus a single replacement with 50% olive oil (OO). In the second dietary trials, salmon were fed FO or a 75% replacement of a blend of rapeseed/linseed and palm oils (75% VO blend) to replicate groups over the whole production cycle from first feeding. In both trials fish were grown to market size and were then fed a FO finishing diet for a further 24 weeks. In salmon, replacement of fish oil (FO) with vegetable oil (VO), up to 100%, did not affect growth and feed conversion. Flesh lipid content was unaffected by dietary lipid although, in liver, lipid was increased in salmon fed > 50% LO but not in salmon fed 75% of the VO blend. Flesh fatty acid concentrations reflected diet fatty acid concentrations, with DHA being highly conserved.
However, in salmon fed 100% VO, flesh DHA & EPA concentrations were reduced by ~65%. It was notable that reduction of DHA and EPA was less in fish fed diets with low PUFA contents, e.g. olive oil, and the VO blend than in fish fed diets high in PUFA e.g. RO & LO. DHA and EPA values could be restored to >80% of the values in salmon fed FO by feeding a 100% FO finishing diet for 16-24 weeks with the duration of the finishing diet period being dependent on fish size, growth rate, and dietary DHA and EPA contents. Therefore, the oils most suited as FO substitutes should be high in monoenes, contain saturate levels similar to those in the fish species being fed and be low in C18 PUFA, especially 18:2n-6, as this fatty acid is poorly oxidised and difficult to remove using finishing diets.
In salmon hepatocytes enzyme activities decrease along the synthetic pathway pathway such that delta-6 fatty acid desaturase (FAD) = C18-20 fatty acid elongase (ELO) > delta-5 FAD > C20-22 ELO > C22-24 ELO = delta-6*FAD. In salmon hepatocytes HUFA synthesis was increased by dietary VO mainly at delta-6 FAD and C18-20 ELO. DHA synthesis as measured by conversion of labelled 18:3n-3 occurred at a low rate in vivo in trout and salmon. DHA synthesis was increased by feeding VO, certainly in trout and possibly also in salmon. However, DHA synthesis was lower in Atlantic salmon parr than in equivalent sized rainbow trout and DHA synthesis decreased, as fish became larger/older. It is notable that, even in fully induced trout, DHA synthesis was insufficient to maintain carcass levels of DHA. The majority of labelled 18:3n-3 (>95%) fed to trout and salmon was oxidized.
The delta-6 FAD, delta-5 FAD and PUFA ELOs were cloned and characterised from salmon. Hepatic delta-6 and delta-5 FAD gene expressions were increased by dietary VO in salmon but ELO expression was increased only in salmon fed LO. Arachidonic acid - derived prostaglandin production was reduced in salmon fed VO diets, although this was less affected when feeding a VO blend than in single VO diets. When salmon were fed a single VO to replace FO, a number of immune parameters (haematocrit, leucocyte numbers, macrophage respiratory burst) were altered by dietary treatment.
However, when a VO blend was chosen to replace FO, non-specific immune functions were not affected up to 75% replacement in salmon. Cataract incidence in salmon fed the 75% VO blend was 4 times higher compared to fish fed FO. Vaccination efficacy against furunculosis in salmon was not affected by the dietary VO while salmon challenged with Vibrio anguillarum did not show significant differences in mortality when FO was replaced by a 75% VO blend.