Dietary supplemental l-Ornithine l-Aspartate reduced lipid deposition and alleviated mitochondrial oxidative stress and inflammatory responses in the liver of broiler chicken.

The liver is the major organ of lipid metabolism in broiler chickens, and disruptions in lipid metabolism can lead to oxidative stress and inflammatory responses, which in turn can cause liver damage, seriously impacting the health of broiler chickens. The following experiment was conducted to investigate the potential effects and related underlying mechanism of l-Ornithine l-Aspartate (OA) on lipid metabolism and inflammatory responses in the livers of broiler chickens fed with a corn-soybean meal basal diet. Dietary addition of OA at 500 mg/kg modulated the AMPK/SREBP1C signaling pathway and down-regulated the relative expression of genes related to lipid synthesis, such as FAS, ACC1, and SCD1, and then reduced the synthesis of fatty acids in the liver and decreased the abdominal fat index, as compared to that of the control group fed with the basal diet. In addition, OA increased mitochondrial membrane oxygen consumption rate, mitigated liver mitochondrial dysfunction, reduced reactive oxygen species production, and decreased inflammatory responses by inhibiting the expression of NF-κB signaling pathway and lowering the levels of inflammatory factors, including IL-1β and TNF-α. In conclusion, dietary OA addition would be not only a therapeutic measure for liver health but also a potential strategy to prevent abdominal fat deposition.