Metabolism of n−3 and n−6 fatty acids in Atlantic salmon liver: Stimulation by essential fatty acid deficiency

• Published in: Lipids
• Main Authors: Ruyter, B., Thomassen, M. S.
• Format: Article in Journal/Newspaper
• Language: English
• Published: Wiley 1999
• Subjects: Atlantic salmon; Salmo salar
• Online Access: http://dx.doi.org/10.1007/s11745-999-0468-3; https://onlinelibrary.wiley.com/doi/full/10.1007/s11745-999-0468-3

Abstract Oxidation, esterification, desaturation, and elongation of [1‐ 14 C]18∶2n−6 and [1‐ 14 C]18∶3n−3 were studied using hepatocytes from Atlantic salmon ( Salmo salar I.) maintained on diets deficient in n−3 and n−6 polyunsaturated fatty acids (PUFA) or supplemented with n−3 PUFA. For both dietary groups, radioactivity from 18∶3n−3 was incoporated into lipid fractions two to three times faster than from 18∶2n−6, and essential fatty acids (FFA) deficiency doubled the incorporation. Oxidation to CO 2 was very low and was independent of substrate or diet, whereas oxidation to acid‐soluble products was stimulated by EFA deficiency. Products from 18∶2n−6 were mainly 18∶3n−6, 20∶3n−6, and 20∶4n−6, with minor amounts of 20∶2n−6 and 22∶5n−6. Products from 18∶3n−3 were mainly 18∶4n−3, 20∶5n−3, and 22∶6n−3, with small amounts of 20∶3n−3. The percentage of 22∶6n−3 in the polar lipid fraction of EFA‐deficient hepatocytes was fourfold higher than in n−3 PUFA‐supplemented cells. This correlated well with our other results obtained after abdominal injection of [1‐ 14 C]18∶3n−3 and [1‐ 14 C]18∶2n−6. In hepatocytes incubated with [4,5‐ 3 H]‐22∶6n−3, 20∶5n−3 was the main product. This retrocon‐version was increased by EFA deficiency, as was peroxisomal β‐oxidation activity. This study shows that 18∶2n−6 and 18∶3n−3 can be elongated and desaturated in Atlantic salmon liver, and that this conversion and the activity of retroconversion of very long chain PUFA is markedly enhanced by FFA deficiency.