Effects of dietary vegetable oil on Atlantic salmon hepatocyte fatty acid desaturation and liver fatty acid compositions.

Fatty acyl desaturase activities, involved in the conversion of the C18 EFA 18:2n-6 and 18:3n-3 to the highly unsaturated fatty acids (HUFA) 20:4n-6, 20:5n-3, and 22:6n-3, are known to be under nutritional regulation. Specifically, the activity of the desaturation/elongation pathway is depressed when animals, including fish, are fed fish oils rich in n-3 HUFA compared to animals fed vegetable oils rich in C18 EFA. The primary aims of the present study were (i) to establish the relative importance of product inhibition (n-3 HUFA) vs. increased substrate concentration (C18 EFA) and (ii) to determine whether 18:2n-6 and 18:3n-3 differ in their effects on the hepatic fatty acyl desaturation/elongation pathway in Atlantic salmon (Salmo salar). Smolts were fed 10 experimental diets containing blends of two vegetable oils, linseed (LO) and rapeseed oil (RO), and fish oil (FO) in a triangular mixture design for 50 wk. Fish were sampled after 32 and 50 wk, lipid and FA composition of liver determined, fatty acyl desaturation/elongation activity estimated in hepatocytes using [1-14C]18:3n-3 as substrate, and the data subjected to regression analyses. Dietary 18:2n-6 was positively correlated, and n-3 HUFA negatively correlated, with lipid content of liver. Dietary 20:5n-3 and 22:6n-3 were positively correlated with liver FA with a slope greater than unity suggesting relative retention and deposition of these HUFA. In contrast, dietary 18:2n-6 and 18:3n-3 were positively correlated with liver FA with a slope of less than unity suggesting metabolism via beta-oxidation and/or desaturation/elongation. Consistent with this, fatty acyl desaturation/elongation in hepatocytes was significantly increased by feeding diets containing vegetable oils. Dietary 20:5n-3 and 22:6n-3 levels were negatively correlated with hepatocyte fatty acyl desaturation. At 32 wk, 18:2n-6 but not 18:3n-3 was positively correlated with hepatocyte fatty acyl desaturation, whereas the reverse was true at 50 wk. The data indicate that both feedback inhibition through increased n-3 HUFA and decreased C18 fatty acyl substrate concentration are probably important in determining the level of hepatocyte fatty acyl desaturation and that 18:2n-6 and 18:3n-3 may differ in their effects on this pathway.