Linoleic acid, α-linolenic acid and enterolactone affect lipid oxidation and expression of lipid metabolism and antioxidant-related genes in hepatic tissue of dairy cows

• Published in: British journal of nutrition 2017-05, Vol.117 (9), p.1199-1211
• Main Authors: Fortin, Émilie, Blouin, Richard, Lapointe, Jérôme, Petit, Hélène V., Palin, Marie-France
• Format: Article
• Language: English
• Subjects: 4-Butyrolactone - analogs & derivatives; 4-Butyrolactone - pharmacology; alpha-Linolenic Acid - pharmacology; Animal Feed - analysis; Animal Nutritional Physiological Phenomena; Animals; Cattle; Diet - veterinary; Fatty Acids; Female; Gene Expression Regulation - drug effects; Lignans - pharmacology; Linoleic Acid - pharmacology; Lipid Peroxidation - drug effects; Liver - drug effects; Liver - metabolism; Molecular Nutrition; Oxidative Stress; Superoxide Dismutase; Thiobarbituric Acid Reactive Substances
• ISSN: 0007-1145; 1475-2662
• DOI: 10.1017/S0007114517000976

Although beneficial effects have been attributed to PUFA supplementation in high-yielding dairy cows, diets rich in PUFA may also increase oxidative stress in tissues such as the liver. To fully exploit the health benefits of PUFA, we believe that the addition of natural antioxidants could help in preventing oxidative damage. Using an in vitro precision-cut liver slices (PCLS) tissue culture system, we investigated the effects of different linoleic acid (LA, n-6):α-linolenic acid (ALA, n-3) ratios (LA:ALA ratio of 4, LA:ALA ratio of 15 and LA:ALA ratio of 25) in the presence or absence of the antioxidant enterolactone (ENL) on (1) the mRNA abundance of genes with key roles in hepatic lipid metabolism, oxidative stress response and inflammatory processes, (2) oxidative damages to lipids and proteins and (3) superoxide dismutase activity in early-lactating dairy cows. The addition of LA and ALA to PCLS culture media increased oxidative damage to lipids as suggested by higher concentrations of thiobarbituric acid reactive substances and increased the expression of nuclear factor erythroid 2-related factor 2 target genes. The addition of ENL was effective in preventing lipid peroxidation caused by LA and ALA. Transcript abundance of sterol regulatory element-binding transcription factor 1 and its lipogenic target genes acetyl-CoA carboxylase α, fatty acid synthase (FASN) and stearoyl-CoA desaturase (SCD) was decreased with LA and ALA, whereas ENL decreased FASN and SCD gene expression. Our results show that addition of LA and ALA to PCLS culture media lowers hepatic lipogenic gene expression and increases oxidative damages to lipids. On the other hand, addition of ENL prevents oxidative damages provoked by these PUFA.