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Effects of dietary vegetable oil on Atlantic salmon hepatocyte fatty acid desaturation and liver fatty acid compositions.
Lipids 2003; 38(7):723-32L

Abstract

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.

Authors+Show Affiliations

Institute of Aquaculture, University of Stirling, Stirling FK9 4LA, Scotland. d.r.tocher@stir.ac.ukNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

14506835

Citation

Tocher, Douglas R., et al. "Effects of Dietary Vegetable Oil On Atlantic Salmon Hepatocyte Fatty Acid Desaturation and Liver Fatty Acid Compositions." Lipids, vol. 38, no. 7, 2003, pp. 723-32.
Tocher DR, Bell JG, Dick JR, et al. Effects of dietary vegetable oil on Atlantic salmon hepatocyte fatty acid desaturation and liver fatty acid compositions. Lipids. 2003;38(7):723-32.
Tocher, D. R., Bell, J. G., Dick, J. R., & Crampton, V. O. (2003). Effects of dietary vegetable oil on Atlantic salmon hepatocyte fatty acid desaturation and liver fatty acid compositions. Lipids, 38(7), pp. 723-32.
Tocher DR, et al. Effects of Dietary Vegetable Oil On Atlantic Salmon Hepatocyte Fatty Acid Desaturation and Liver Fatty Acid Compositions. Lipids. 2003;38(7):723-32. PubMed PMID: 14506835.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of dietary vegetable oil on Atlantic salmon hepatocyte fatty acid desaturation and liver fatty acid compositions. AU - Tocher,Douglas R, AU - Bell,J Gordon, AU - Dick,James R, AU - Crampton,Viv O, PY - 2003/9/26/pubmed PY - 2004/5/1/medline PY - 2003/9/26/entrez SP - 723 EP - 32 JF - Lipids JO - Lipids VL - 38 IS - 7 N2 - 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. SN - 0024-4201 UR - https://www.unboundmedicine.com/medline/citation/14506835/Effects_of_dietary_vegetable_oil_on_Atlantic_salmon_hepatocyte_fatty_acid_desaturation_and_liver_fatty_acid_compositions_ L2 - https://link.springer.com/article/10.1007/s11745-003-1120-y DB - PRIME DP - Unbound Medicine ER -