Effect of different fat sources and vitamin E status/levels on growth performance, antioxidant status, carcass characteristics, fatty acid profile, and meat quality of pigs grown to heavy slaughter weight at 150 kg

Abstract

Abstract Two experiments were used to evaluate the potential interaction of fat source and vitamin E (VE) in heavy slaughter weight pigs. In Experiment 1, a total of 64 individually-fed pigs (28.41 ± 0.83 kg) were randomly assigned to 8 dietary treatments in a 4×2 factorial arrangement. Fat treatments included cornstarch (CS), tallow (TW), corn-oil (CO), and coconut-oil (CN). VE treatments were dietary α-tocopheryl-acetate (ATA) at 11 and 200 ppm. In Experiment 2, a total of 72 individually fed pigs (28.55 ± 1.16 kg) were randomly assigned to 12 dietary treatments in a 2×6 factorial arrangement. Fat treatments were TW and CO. VE treatments included four levels of ATA (11, 40, 100, and 200 ppm) and two levels of mixed tocopherols (primarily γ-tocopherol; 40 and 100 ppm). VE deposition, growth performance, and meat quality were measured in both experiments. In both experiments, interaction between fat sources and VE were detected (P < 0.01) on plasma VE concentration, which increased (P < 0.01) with time and with increasing dietary VE, but increased faster (P < 0.05) in pigs fed with CN and TW compared to pigs fed CS and CO. Compared to CO, more saturated dietary fat sources (CN and TW) led to firmer belly (P < 0.01), which had more (P < 0.01) SFA and MUFA while less (P < 0.01) PUFA. In Experiment 1, increasing dietary ATA decreased (P < 0.05) FCR in Phase 4 and Phase 5. In Experiment 2, increasing dietary ATA increased overall ADG (linear, P = 0.02), with an interaction (P < 0.05) with fat sources on cumulative ADG during Phase1-4, wherein pigs fed CO, but not TW, had increased ADG with increasing dietary ATA. Increasing dietary ATA increased (quadratic, P < 0.05) liver SOD activity, and decreased (quadratic, P < 0.05) liver MDA content. The oxidative stability of loin was improved (P < 0.01) when dietary ATA increased over 40 ppm. In summary, both dietary fat source and VE supplementation affected the response measures.