and higher levels of
the fatty acids that were abundant in the alternative lipids compared
to those of fish fed the FISH diet (22.1 g n-3 fatty acids/100 g FAME;
20.7 g LC-PUFAs/100 g FAME). Fillets of fish fed the SFA SOY diet exhibited
higher levels of SFAs, particularly 16:0, compared to other dietary
treatments (44.2 vs. 33.6–40.8 g SFAs/100 g FAME; 32.8 vs. 23.4–
30.1 g 16:0/100 g FAME). Fillets of fish fed the MUFA SOY diet presented
significantly elevated levels of MUFAs, particularly 18:1n-9, in comparison
with fillets of fish fed the other diets (44.6 vs. 29.4–36.8 g MUFAs/
100 g FAME; 36.6 vs. 18.2–27.2 g 18:1n-9/100 g FAME). Fillets of fish fed
the C18 PUFA SOY diet contained higher levels of n-6 and C18 PUFAs, particularly
18:2n-6, compared to fillets of fish fed the other diets (21.2 vs.
7.3–11.5 g n-6 fatty acids/100 g FAME; 23.7 vs. 8.3–12.6 g C18 PUFAs/
100 g FAME; 20.7 vs. 6.7–10.9 g 18:2n-6/100 g FAME). Although not
as enriched as fillets from the MUFA SOY and C18 PUFA SOY treatments,
fillets of fish fed the PALM and POULTRY diets also contained higher
levels of MUFAs, n-6 fatty acids, and C18 PUFAs. These trends were
observed, albeit to a lesser extent in liver (Table 5) and eye tissues
(Table 6), but not in brain tissue (Table 7), which was relatively resistant
to diet-induced compositional change. As illustrated by the ranges
of Djh values observed, tissue fatty acid profile distortion was greatest
among fish fed the MUFA SOY and C18 PUFA SOY diets, least overt
among fish fed the SFA SOY diet, and intermediate among fish fed the
PALM and POULTRY diets (Fig. 2). Although the SFA SOY diet deviated
most greatly from the FISH diet in terms of fatty acid composition, it
yielded the lowest degree of tissue profile modification. Across dietary
treatments, fillet (Djh = 8.9–19.7), liver (Djh = 7.3–16.5), and eye
tissues (Djh = 8.3–18.9) exhibited higher Djh ranges than brain tissues
(Djh = 2.8–3.2) (Fig. 2). Fillet and liver total lipid content did not vary
significantly among dietary treatments