, most likely because this level of

, most likely because this level of sparing
is ‘safe’ and unlikely to reduce dietary LC-PUFA content below levels
required by most species. Fatty acid requirements are often reported
in terms of fatty acid groupings, such as the combined EPA and/or
DHA requirement reported by the National Research Council (referred
to as a “n-3 LC-PUFA” requirement; NRC, 2011). According to this reference, the combined EPA/DHA requirements of marine finfish
(though not specifically Florida Pompano) range from 5 to 15 g/kg
diet (0.5–1.5%; NRC, 2011). In the present study, the FISH diet contained
14 g EPA/kg and 11 g DHA/kg (totaling 25 g/kg or 2.5% of the diet),
whereas the experimental diets contained 6–8 g EPA/kg and 5–7 g
DHA/kg (totaling 11–15 g/kg or 1.1–1.5% of the diet) (Table 2; calculated
amounts based on dietary fatty acid profile, 0.93 g of FAME/g of lipid
conversion, and the crude dietary lipid content). Thus, all of our diets
met or exceeded the lower end of the requirement range, at least in
terms of combined EPA/DHA content, and expectedly supported good
growth and 100% survival. Although significant treatment effects were
noted for FCR, feed intake, and HSI, it is unlikely that these differences
represent cause for serious concern from a biological or practical perspective.
These differences are most likely related to minor differences
in feed palatability or digestibility rather than nutrient (i.e., essential
fatty acid) deficiency.
With respect to tissue fatty acid profile, all tissues analyzed were affected
by dietary treatments, and generally mirrored dietary fatty acid
composition. This finding is highly consistent with the fish oil sparing
literature (Turchini et al., 2009). All experimental diets yielded fillets
with reduced levels of beneficial n-3 fatty acids and LC-PUFAs compared
to the FISH control group (Table 4). The alternative lipids tested lacked
n-3 LC-PUFAs, but contained high levels of SFAs, MUFAs, and/or C18
PUFAs. As expected, tissues of fish fed the alternative lipid-based feeds
began to more closely resemble the feeds themselves. For example,
fish fed C18 PUFA SOY and MUFA SOY feeds exhibited elevated deposition
of the eponymous fatty acids types, primarily 18:2n-6 and 18:1n-
9, respectively. Although less compositionally distinct, the POULTRY
feed contained less n-3 LC-PUFAs and more C18 PUFAs, MUFAs, and
SFAs, yielding similar shifts in tissue composition, particularly in the fillet
tissue. However, this effect was less overt with feeds containing
higher dietary levels of SFAs: the abundance of SFAs in the SFA SOY
and PALM feeds did not translate to proportional enrichment of these
fatty acids in the tissues (Fig. 2).
It is becoming increasingly evident that some fatty acids interfere
with the availability and tissue deposition of LC-PUFAs, whereas others
may have the opposite effect. In most cases, C18 PUFA-rich feeds appear
to reduce the availability and deposition of LC-PUFAs in the tissues.
Conversely, in some taxa, feed formulations rich in SFAs appear advantageous
in terms of maintaining tissue fatty acid profile (i.e., attenuating
reductions in LC-PUFA content typically associated with fish oil sparing/
replacement) and, in some cases, effectively reducing the amount of LCPUFAs
needed in the diet to satisfy requirements for these nutrients and
support tissue enrichment