The effects of linoleic acid (LA) and α-linolenic acid (ALA) as precur-sor and inhibitor in the chain of n-3 and n-6 polyunsaturated fatty acids (LC PUFA) were studied in liver and brain of growing pigs (15-30 kg BW). In a 2x2 factorial arrangement, 32 gilts from 4 litters were assigned to one of four dietary treatments, varying in LA and ALA intake. Differences between low and high intake were designed to be identical for LA and ALA: Low ALA and LA intakes were 0.15 and 1.30, and high ALA and LA intakes were 1.45 and 2.60 g/(kg BW0.75/d), respectively. Intakes of saturated and monounsaturated FA, and other nutrients were kept constant. Consequently, energy intake increased with LA and ALA additions. After 28d on the dietary treatments, pigs were sacrificed. Liver and brain tissues were sampled and analyzed for FA composition and mRNA levels of Δ5 and Δ6 desaturase and elon-gase 2 and 5. In the liver, LA intake substantially increased C20:4n-6 (ARA) and ALA intake increased C20:5n-3 (EPA) concentrations, but decreased C22:6n-3 (DHA) (all P<0.01). Competition between n-3 and n-6 pathways was evidenced by substantial reductions of ARA at high ALA intakes (>40%) and EPA (>35%) and DHA (>20%) by increased LA intake (all P<0.001). Liver mRNA levels of Δ5 and Δ6 desaturase were increased by LA intake, and elongase 2 by both ALA and LA (P<0.01). Brain DHA was virtually unaffected by the dietary treat-ments, but C22:5n-3 was increased by ALA and decreased by LA (all P<0.001). mRNA levels of Elongase 2 were increased by ALA intake. In conclusion, ALA is a strong regulator in both the n-3 and n-6 LC PUFA chains. In addition to desaturation (Δ6), elongation from EPA and ARA may be rate limiting in brain and liver. Finally, brain DHA is virtually unaffected by ALA and LA.
|Journal||Journal of Dairy Science|
|Issue number||E-suppl 1|
|Publication status||Published - 2009|