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with 16:0, 16:1 and 18:1n-9 (Henderson 1996; Kiessling and Keissling 1993;
Frøyland et al. 2000), although it should be noted that much of this work was done
using tissue homogenates, isolated cells or mitochondria. In our recent studies, 16:0
was selectively deposited in flesh, suggesting that it may not be readily used as a
catabolic substrate (Bell et al. 2003a, 2004a; Table 6.1). By comparison, 18:1n-9
was selectively deposited except when present in high concentrations, e.g., where
salmonids were fed > 33% RO or OO (Torstensen et al. 2004a,b) and in sea bass
and bream fed 60% RO and 60% OO (Izquierdo et al. 2005; Mourente et al. 2005).
It is generally accepted that DHA is selectively retained due to the biological
importance of this fatty acid in cell membrane functional integrity, especially in
neural, reproductive and immune tissues (Sargent et al. 2002). The selective
deposition of 16:0 and 18:1n-9, rather than mobilisation, may reflect the structural
importance of both these fatty acids in membrane phospholipids, where they are
often located in the sn-1 position, especially in PC and PE, with PUFA and HUFA
being favoured in the sn-2 position (Bell and Dick 1991; Sargent et al. 2002).
The health benefits of fish consumption, related to the n-3 HUFA content, are now
widely recognised (Simopoulos 1999; Connor 2000) and it is important that
aquaculture maintains a healthy product image by producing seafood that is comparable
with those from capture fisheries. However, evidence from several studies suggests
that when fish are cultured on diets containing VO, especially at levels over 50%, then
there are significant reductions in flesh EPA and DHA (Table 6.2, Bell et al. 2004a;
Torstensen et al. 2004a,b; Menoyo et al. 2004; Mourente et al. 2005). To overcome
this, fish can be placed on a FO finishing diet for a period prior to harvest to restore
n-3 HUFA levels. In general, the ability to restore EPA and DHA concentrations
was more easily achieved than the dilution or wash out of the 18:2n-6 and 18:3n-3
(Bell et al. 2004a; Torstensen et al. 2004b, 2005; Mourente et al. 2005; Izquierdo
et al. 2005). In salmon and trout, although DHA and EPA levels were still
significantly lower, after 24 and 12 weeks on a FO finishing diet, respectively, the
values attained were at least 80% of the values in fish fed FO, in fish previously fed
VO compared to fish fed FO throughout. In salmon, the DHA and EPA were largely
restored after 16 weeks with only further small increases up to 24 weeks (Bell et al.
2004a) while for sea bass and bream restoration of EPA and DHA could be largely
achieved in 14 weeks (Mourente et al. 2005; Izquierdo et al. 2005).
In trials where fish were fed what were considered maximal levels of VO
(60–100% of total added oil) for the whole production cycle, fish were exposed to high
dietary VO for an extended period of time of 50–100 weeks. However, the blend
of RO, LO and PO used was selected to balance the saturated, monounsaturated and
polyunsaturated fatty acids with the same levels as found in either capelin oil or
anchovy oil. This generally resulted in lower levels of 18:2n-6 and 18:3n-3 than
were found when either LO or RO were used as single FO substitutes. In salmon,
flesh DHA and EPA levels were restored to ~90%, in fish fed 75% VO, and ~65%,
in fish fed 100% VO, of values in fish fed FO throughout, after 24 weeks on a FO
finishing diet (Torstensen et al. 2005). The difference between the two VO treatments can be explained, in part, by the seasonal differences in the finishing diet
period between the 75% VO trial in Scotland (March–September when water
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