Please use this identifier to cite or link to this item: http://hdl.handle.net/1893/2931
Appears in Collections:Aquaculture Journal Articles
Peer Review Status: Refereed
Title: Effects of dietary vegetable oil on atlantic salmon hepatocyte fatty acid desaturation and liver fatty acid compositions
Author(s): Tocher, Douglas R
Bell, J Gordon
Dick, James R
Crampton, Viv
Contact Email: drt1@stir.ac.uk
Keywords: Atlantic salmon
Salmo salar
Fish oil
Vegetable oil
Linseed oil
Rapeseed oil
Mixture design
Liver
Hepatocytes
Lipid metabolism
Polyunsaturated fatty acid
biosynthesis
Desaturation
Elongation
Atlantic salmon
Lipids in nutrition
Fishes Feeding and feeds
Issue Date: Jul-2003
Date Deposited: 14-Apr-2011
Citation: Tocher DR, Bell JG, Dick JR & Crampton V (2003) Effects of dietary vegetable oil on atlantic salmon hepatocyte fatty acid desaturation and liver fatty acid compositions. Lipids, 38 (7), pp. 723-732. http://www.springerlink.com/content/0024-4201/; https://doi.org/10.1007/s11745-003-1120-y
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-3HUFA compared to animals fed vegetable oils rich in C18 EFA. The primary aims of the present study were a) to establish the relative importance of product inhibition (n-3HUFA) versus increased substrate concentration (C18 EFA) and, b) 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 ten 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 weeks. Fish were sampled after 32 and 50 weeks, lipid and fatty acid 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-3HUFA negatively correlated, with lipid content of liver. Dietary 20:5n-3 and 22:6n-3 were positively correlated with liver fatty acids 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 fatty acids with a slope of less than unity suggesting metabolism via β-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 weeks, 18:2n-6 but not 18:3n-3, was positively correlated with hepatocyte fatty acyl desaturation activity whereas the reverse was true at 50 weeks. The data indicate that both feedback inhibition through increased n-3HUFA and decreased C18 fatty acyl substrate concentration are probably important in determining hepatocyte fatty acyl desaturation activities, and that 18:2n-6 and 18:3n-3 may differ in their effects on this pathway.
URL: http://www.springerlink.com/content/0024-4201/
DOI Link: 10.1007/s11745-003-1120-y
Rights: Published in Lipids by Springer / American Oil Chemists' Society (AOCS).; The final publication is available at www.springerlink.com

Files in This Item:
File Description SizeFormat 
EWos VO Liver final.pdfFulltext - Accepted Version674.66 kBAdobe PDFView/Open



This item is protected by original copyright



Items in the Repository are protected by copyright, with all rights reserved, unless otherwise indicated.

The metadata of the records in the Repository are available under the CC0 public domain dedication: No Rights Reserved https://creativecommons.org/publicdomain/zero/1.0/

If you believe that any material held in STORRE infringes copyright, please contact library@stir.ac.uk providing details and we will remove the Work from public display in STORRE and investigate your claim.